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1.  Distribution of radioactivity from 14C-formaldehyde in pregnant mice and their fetuses. 
The distribution of 14C after the administration of 14C-formaldehyde was studied in pregnant mice by a whole body low temperature autoradiographic technique. The concentrations of formaldehyde and its metabolites in maternal and fetal blood and tissues were determined in unsectioned tissues by liquid scintillation spectrophotometry. The binding of 14C from 14C-formaldehyde to cells and DNA in maternal and fetal mouse liver was also measured. Radioactivity of 14C deriving from 14C-formaldehyde was found immediately after injection, and showed strong accumulation and retention three hours after injection. The organs that had high concentrations at all studied survival intervals were maternal liver, intestinal mucosa, bone marrow, kidneys, and salivary glands. Considerable amounts of radioactivity were found in the fetuses at six hours after injection, and the concentrations were almost the same as in the maternal tissues. The elimination of 14C-formaldehyde and metabolites from the placenta and fetus occurred more slowly than from maternal tissue.
PMCID: PMC1061257  PMID: 8435351
2.  Distribution of aztreonam into fetuses and milk of rats. 
Subcutaneous administration of [14C]aztreonam (150 mg/kg) to pregnant rats was followed by the appearance of radioactive moieties in fetuses and amniotic fluid. Concentrations of both total radioactivity and unchanged aztreonam in maternal serum declined more rapidly than those in fetuses and amniotic fluid. [14C]aztreonam (150 mg/kg) was also administered subcutaneously to lactating rats. Radioactivity and unchanged aztreonam were found in the suckling pups and in the serum and milk of the dam. Results obtained by whole-body autoradiography were generally consistent with these obtained by measuring radioactivity present in the excised tissues. Autoradiographs of the pups showed detectable amounts of radioactivity in the brain; since no radioactivity was detectable in the brain of the dam, it appears that the blood-brain barrier was not fully developed in 7-day-old pups.
PMCID: PMC284105  PMID: 6541451
3.  Distribution of pimonidazole and RSU 1069 in tumour and normal tissues. 
British Journal of Cancer  1990;62(6):915-918.
The tritium-labelled analogues of pimonidazole and RSU 1069 were injected into mice bearing the KHT murine sarcoma which has a hypoxic cell fraction of approximately 10%. The distribution of activity at 24 h was recorded using autoradiography and measurement of tissue activity. Autoradiographs with both drugs showed high activity in particular cells within tumour, eye (melanin-associated cells), eyelid (Meibomian gland), liver (centrilobular area), skin (sebaceous gland and melanin), stomach (squamous area), footpad, oesophagus, labial gland, Zymbal's gland, preputial gland, parotid gland (intralobular ducts) and airway epithelium. These tissues had previously been identified as sites of binding of misonidazole. The measurement of total tissue radioactivity showed significantly higher activity in liver, eyelid (Meibomian gland), oesophageal lining, kidney and labial gland than was found in the tumour.
PMCID: PMC1971577  PMID: 2257219
4.  Lead Poisoning-Induced Hypertensive Crisis Managed by Prazosin: A Case Report 
Chronic lead exposure is known to be a risk factor for hypertension (HTN). No specific medication is recommended for the treatment of lead-induced hypertension (LIHTN).
Case Presentation
Our patient was a male admitted with the chief complaint of chronic abdominal pain. His whole blood lead level was reported to be 1961 µg/L. He also mentioned a previous history of HTN managed by propranolol (10 mg, TDS). He discharged himself by giving written consent and 19 days later, he was re-admitted due to high blood pressure of 220/140 mmHg. His Blood pressure (BP) was decreased to 180/110 mmHg with sublingual captopril; but, in maintenance therapy, higher doses of captopril could not further decrease BP. Amlodipine was tried which was discontinued due to the patient intolerance. Prazosin was then administered in gradual increasing doses up to 1 mg twice a day and captopril was tapered.
We would like to suggest that LIHTN may better be managed by alpha blockers compared with converting enzyme inhibitors
PMCID: PMC3840843  PMID: 24349754
Lead; Hypertension; Prazosin
5.  Reduced brain glucose with normal plasma glucose in salicylate poisoning 
Journal of Clinical Investigation  1970;49(11):2139-2145.
After the intraperitoneal injection into young mice of 700-800 mg/kg of salicylate, brain glucose fell to one-third or less of control values despite normal plasma glucose levels; brain lactate was nearly doubled and there were small decreases in phosphocreatine (18%) and in glycogen (17%). ATP, pyruvate, α-ketoglutarate, and glutamate were unchanged. In liver, glycogen was reduced 79% and lactate was five times higher than in control animals; glucose, glucose-6-phosphate, and ATP were unchanged.
Since salicylate uncouples oxidative phosphorylation, it is postulated that high energy phosphate in the brain is maintained near normal levels by a compensatory increase in cerebral glycolysis. Apparently the brain glucose level falls because the rate of utilization exceeds the rate at which glucose can be supplied from the blood. Concurrent administration of glucose with salicylate elevated brain glucose concentration and was associated with striking improvement in the condition and the increased survival of the animals. These findings stress the fact that in salicylate poisoning the supply of glucose to the brain may be inadequate even when blood glucose levels are normal.
PMCID: PMC535789  PMID: 4319971
6.  Distribution of [14C]aztreonam in rat tissue. 
[14C]aztreonam was administered intramuscularly (50 mg/kg) to male and female rats. Groups of 10 rats (five male and five female) were sacrificed at 0.25, 2, 6, and 24 h after dosing. Blood and various tissues were removed from six rats (three male and three female) in each group for determination of total radioactivity and unchanged aztreonam by liquid scintillation counting and thin-layer radiochromatography. The remaining rats were prepared for whole-body autoradiography. Radioactivity was distributed rapidly to most tissues and was rapidly eliminated from blood into urine and bile. Concentrations of total radioactivity in kidney, liver, small and large intestines and their contents, and urinary bladder were higher than those in serum at all the times examined. Concentrations of unchanged aztreonam in serum, kidney, liver, and lung declined at about the same rate as did that of total radioactivity in the same tissues. The results of whole-body autoradiography essentially confirmed the results of the distribution of [14C]aztreonam as determined by liquid scintillation counting. No major differences between males and females were observed when concentrations in organs common to both were compared.
PMCID: PMC284104  PMID: 6541450
7.  Toad venom poisoning: resemblance to digoxin toxicity and therapeutic implications 
Heart  2003;89(4):e14.
A healthy man developed gastrointestinal symptoms after ingesting purported aphrodisiac pills. He had severe unrelenting bradycardia, hyperkalaemia, and acidosis. He rapidly developed severe life threatening cardiac arrhythmias and died after a few hours. He was found to have positive serum digoxin concentrations, although he was not taking digoxin. Toad venom poisoning is similar to digitalis toxicity and carries a high mortality. Cardiac glycoside poisoning can occur from ingestion of various plants and animal toxins, and the venom gland of cane toad (Bufo marinus) contains large quantities of cardiac glycosides. Toad venom, a constituent of an aphrodisiac, was considered responsible for the development of clinical manifestations and death in this patient. Digoxin specific Fab fragment has been reported to be beneficial in the treatment of toad venom poisoning. This report alerts physicians to the need to be aware of a new community toxic exposure, as prompt treatment with digoxin specific Fab fragment may be life saving. The treatment approach to patients with suspected toad venom poisoning is described.
PMCID: PMC1769273  PMID: 12639891
toad venom poisoning; digoxin specific Fab fragments; aphrodisiac; toxicology
8.  In vitro incorporation of (3H)threonine and (3H)glucose by the mucous and serous cells of the human bronchial submucosal gland. A quantitative electron microscope study 
The Journal of Cell Biology  1975;67(2):320-344.
Incorporation of [3H]threonine and [3H]glucose by the mucous and serous cells of the human bronchial submucosal gland has been studied over 8 h using, for the first time in vitro pulse labeling and electron microscope autoradiography. In assessing the autoradiographs, two methods were compared, the circle analysis and the recently described hypothetical grain analysis. Preliminary studies showed formaldehyde to be the most suitable fixative. Chemical analysis of tissue revealed that [3H]threonine was incorporated into the polypeptide moiety of the bronchial gland product and that metabolites of [3H]-glucose were incorporated into the carbohydrate. Tritiated threonine was first localized in the endoplasmic reticulum of both mucous and serous cells and later migrated to the Golgi apparatus, while metabolites of [3H]glucose localized first mainly in the Golgi apparatus. From here, both radioactive precursors were next identified in vacuoles and, finally, in secretory granules. The mucous cell incorporated strikingly more of both radioactive precursors than the serous cell. Thus, it seems that oligosaccharides of mucous and serous cell glycoproteins are synthesized mainly in the Golgi apparatus and added there to the polypeptide core which is synthesized in the endoplasmic reticulum. The relationship of the mucous cell to the serous cell is discussed. It seems that under "normal" conditions each cell represents a different line but that injury may transform a serous cell into a mucous cell.
PMCID: PMC2109595  PMID: 1194352
9.  Clinical Chemistry of Staphylococcal Enterotoxin Poisoning in Monkeys 
Applied Microbiology  1966;14(3):445-450.
Clinical chemistry values were examined in 90 monkeys administered a purified preparation of staphylococcal enterotoxin, type B, intravenously. These studies showed an early release of epinephrine accompanied by a mild increase in blood glucose. This was followed by progressively developing prolonged hypoglycemia. An early increase in bloodurea nitrogen occurred, presumably as a result of both prerenal azotemia and functional renal failure seen in association with the observed hypotension. Serum protein, Ca, and Cl concentrations decreased with time. Pi levels increased, whereas Na and K concentrations in serum remained unchanged. Serum enzyme concentrations were unchanged, with the exception of serum glutamic oxaloacetic transaminase, which rose rapidly when compared with prechallenge control observations or with values from sham-challenged monkeys. These changes were statistically significant. These results suggested that enterotoxin administered intravenously produced early change in glucose metabolism, possibly related initially to catecholamine release and later to increased utilization of glucose and metabolic acidosis. Other findings were compatible with tissue breakdown at as yet undetermined locations and with loss of endothelial membrane integrity, as evidenced by loss of protein from the vascular space.
PMCID: PMC546739  PMID: 4961554
10.  Choice of poison for intentional self-poisoning in rural Sri Lanka 
Although intentional self-poisoning is a major public health problem in rural parts of the Asia-Pacific region, relatively little is known of its epidemiology. We aimed to determine why Sri Lankan self-poisoning patients choose particular poisons, and whether acts of self-harm with highly dangerous poisons were associated with more premeditation and effort.
We interviewed 268 self-poisoning patients presenting to two district general hospitals in rural Sri Lanka.
85% of patients cited easy availability as the basis for their choice of poison. There was little premeditation: more than 50% ingested the poison less than 30 minutes after deciding to self-harm. Patients had little knowledge about treatment options or lethality of the poison chosen. We found no difference in reasons for choice of poison between people ingesting different poisons, despite marked differences in toxicity, and between people who died and those who survived.
Poisons were chosen on the basis of availability, often at short notice. There was no evidence that people using highly toxic poisons made a more serious or premeditated attempt. Restrictions on availability of highly toxic poisons in rural communities must be considered in strategies to reduce the number of intentional self-poisoning deaths in the Asia Pacific region.
PMCID: PMC1940039  PMID: 16749546
To determine the role of RLIP76 in providing protection from radiation and chemotherapy. In the present report, we used RLIP76 to refer to both the mouse (Ralbp1) and the human (RLIP76) 76-kDa splice variant proteins (RLIP76) for convenience and to avoid confusion. In other reports, Ralbp1 refers to the mouse enzyme (encoded by the Ralbp1 gene), which is structurally and functionally homologous to RLIP76, the human protein encoded by the human RALBP1 gene.
Methods and Materials
Median lethal dose studies were performed in RLIP76-/- and RLIP76+/+ C57B mice after treatment with a single dose of RLIP76 liposomes 14 h after whole body radiation. The radiosensitivity of the cultured mouse embryonic fibroblasts and the effects of buthionine sulfoximine (BSO), amifostine, c-jun N-terminal kinase (JNK), protein kinase B (Akt), and MAPK/ERK kinase (MEK) were determined by colony-forming assays. Glutathione-linked enzyme activities were measured by spectrophotometric assays, glutathione by dithiobis-2-nitrobenzoic acid (DTNB), lipid hydroperoxides by iodometric titration, and aldehydes and metabolites by thiobarbitauric acid reactive substances and liquid chromatography-mass spectrometry (LCMS).
RLIP76-/- mice were significantly more sensitive to radiation than were the wild-type, and RLIP76 liposomes prolonged survival in a dose-dependent manner in both genotypes. The levels of 4-hydroxynonenal and glutathione-conjugate of 4-hydroxynonenal were significantly increased in RLIP76-/- tissues compared with RLIP76+/+. RLIP76-/- mouse embryonic fibroblasts were markedly more radiosensitive than RLIP76+/+ mouse embryonic fibroblasts, despite increased glutathione levels in the former. RLIP76 augmentation had a remarkably greater protective effect compared with amifostine. The magnitude of effects of RLIP76 loss on radiation sensitivity was greater than those caused by perturbations of JNK, MEK, or Akt, and the effects of RLIP76 loss could not be completely compensated for by modulating the levels of these signaling proteins.
The results of our study have shown that RLIP76 plays a central role in radiation resistance.
PMCID: PMC2664086  PMID: 18793957
RLIP76; Ralbp1; Radiation-resistance; Embryonic fibroblasts
12.  Organophosphorus poisoning (acute) 
Clinical Evidence  2007;2007:2102.
Key Points
Acetylcholinesterase inhibition by organophosphorus pesticides or nerve gases can cause acute parasympathetic system dysfunction, muscle weakness, seizures, coma, and respiratory failure. Prognosis depends on the dose and relative toxicity of the specific compound, as well as pharmacokinetic factors.
Initial resuscitation, then atropine and oxygen, are considered to be the mainstays of treatment, although good quality studies to show benefit have not been found. We don't know the optimum dose of atropine to give, but common clinical practice is to administer sufficient to keep the heart rate greater than 80 beats per minute, systolic blood pressure above 80mmHg, and the lungs clear. Glycopyrronium bromide may be as effective as atropine in preventing death, with fewer adverse effects, although no adequately powered studies have been done.
Washing the poisoned person and removing contaminated clothes is a sensible approach, but no studies have been done to evaluate benefit. Healthcare workers should ensure that washing does not distract them from other treatment priorities, and should protect themselves from contamination.
Benzodiazepines are considered to be standard treatment to control organophosphorus induced seizures, although no studies have been found.
We don't know whether activated charcoal, alpha2 adrenergic receptor agonists (clonidine), butyrylcholinesterase replacement therapy using fresh frozen plasma or plasmapheresis, magnesium sulphate, N-methyl-D-aspartate receptor antagonists, organophosphorus hydrolases, sodium bicarbonate, milk and other "home remedies" taken soon after ingestion, cathartics, or extracorporeal clearance improve outcomes. Oximes have not been shown to improve outcomes, but studies have been of poor quality so a definite conclusion cannot be made.Potential benefits from gastric lavage or ipecacuanha are likely to be outweighed by the risks of harm, such as aspiration.
PMCID: PMC2943818  PMID: 19454054
13.  Differences in Susceptibility to Okadaic Acid, a Diarrhetic Shellfish Poisoning Toxin, between Male and Female Mice 
Toxins  2012;5(1):9-15.
The mouse bioassay (MBA) for diarrhetic shellfish poisoning (DSP) toxins has been widely used in many countries of the world. In the Japanese and EU methods, male mice are designated to be used for MBA. Female mice were described to be less susceptible than male mice. To the best of our knowledge, however, there have been no reports on the details of sex differences in susceptibility to DSP toxins. In this study, we investigated whether, and to what extent, female mice are less sensitive to DSP toxins. A lethal dose of okadaic acid (OA), one of the representative DSP toxins, was injected intraperitoneally into mice. The mice were observed until 24 hours after injection. Both male and female mice of ICR and ddY strains, which are designated in the Japanese official method, were compared. All the mice were four weeks old and weighed 18–20 g. The experiments were repeated twice. The lethality was 70%–100%. Survival analysis showed no sex differences in susceptibility to OA, but ICR female mice showed significant resistance compared with other groups in one out of two trials. These results indicate that sex differences were not clear but, nonetheless, male mice showed more stable results.
PMCID: PMC3564064  PMID: 23271638
sex difference; okadaic acid; mouse bioassay; diarrhetic shellfish poisoning (DSP) toxin
14.  Detection of Diarrheic Shellfish Poisoning and Azaspiracid Toxins in Moroccan Mussels: Comparison of the LC-MS Method with the Commercial Immunoassay Kit 
Marine Drugs  2008;6(4):587-594.
Diarrheic shellfish poisoning (DSP) is a recurrent gastrointestinal illness in Morocco, resulting from consumption of contaminated shellfish. In order to develop a rapid and reliable technique for toxins detection, we have compared the results obtained by a commercial immunoassay-“DSP-Check” kit” with those obtained by LC-MS. Both techniques are capable of detecting the toxins in the whole flesh extract which was subjected to prior alkaline hydrolysis in order to detect simultaneously the esterified and non esterified toxin forms. The LC-MS method was found to be able to detect a high level of okadaic acid (OA), low level of dinophysistoxin-2 (DTX2), and surprisingly, traces of azaspiracids 2 (AZA2) in mussels. This is the first report of a survey carried out for azaspiracid (AZP) contamination of shellfish harvested in the coastal areas of Morocco. The “DSP-Check” kit was found to detect quantitatively DSP toxins in all contaminated samples containing only OA, provided that the parent toxins were within the range of detection and was not in an ester form. A good correlation was observed between the two methods when appropriate dilutions were performed. The immunoassay kit appeared to be more sensitive, specific and faster than LC-MS for determination of DSP in total shellfish extract.
PMCID: PMC2630846  PMID: 19172196
Diarrheic shellfish poisoning; Okadaic acid; LC/MS; ELISA; Dinophysistoxin 2; Dinophysis spp.; azaspiracids toxins
15.  Cobinamide is superior to other treatments in a mouse model of cyanide poisoning 
Cyanide is a rapidly acting cellular poison, primarily targeting cytochrome c oxidase, and is a common occupational and residential toxin, mostly via smoke inhalation. Cyanide is also a potential weapon of mass destruction, with recent credible threats of attacks focusing the need for better treatments, since current cyanide antidotes are limited and impractical for rapid deployment in mass casualty settings.
We have used mouse models of cyanide poisoning to compare the efficacy of cobinamide, the precursor to cobalamin (vitamin B12), to currently approved cyanide antidotes. Cobinamide has extremely high affinity for cyanide and substantial solubility in water.
Materials and Methods
We studied cobinamide in both an inhaled and intraperitoneal model of cyanide poisoning in mice.
We found cobinamide more effective than hydroxocobalamin, sodium thiosulfate, sodium nitrite, and the combination of sodium thiosulfate-sodium nitrite in treating cyanide poisoning. Compared to hydroxocobalamin, cobinamide was 3 and 11 times more potent in the intraperitoneal and inhalation models, respectively. Cobinamide sulfite was rapidly absorbed after intramuscular injection, and mice recovered from a lethal dose of cyanide even when given at a time when they had been apneic for over two minutes. In range finding studies, cobinamide sulfite at doses up to 2000 mg/kg exhibited no clinical toxicity.
Discussion and Conclusion
These studies demonstrate that cobinamide is a highly effective cyanide antidote in mouse models, and suggest it could be used in a mass casualty setting, because it can be given rapidly as an intramuscular injection when administered as cobinamide sulfite. Based on these animal data cobinamide sulfite appears to be an antidote worthy of further testing as a therapy for mass casualties.
PMCID: PMC3119202  PMID: 20704457
Antidote; Poisoning management; Poisoning; Hydroxocobalamin
16.  The Pathology of Arylmercurial Poisoning in Swine 
To produce arylmercurial poisoning, phenylmercuric chloride (PMC) was administered daily to 30 healthy five week-old piglets for periods of up to 90 days. The dosage used ranged from 0.19 to 4.56 mg of mercury (Hg)/kg. Levels exceeding 2.28 mg Hg/kg daily were moderately toxic.
The disease occurring in this intoxication resulted from injury to the kidneys and large intestine. Fetid diarrhea and failure to gain weight were consistent clinical signs. The primary gross lesions were necrotic typhlitis and colitis, and nephrosis. Degeneration and necrosis were found in affected organs. Regeneration was prominent in the proximal convoluted tubules.
The pathology of this disease was similar to that described for mercuric chloride poisoning in other species and, presumably, reflected the ease with which PMC was metabolized to release mercuric ion.
Tissue analysis for mercury suggested that only certain target organs, such as kidney and colon, accumulated significantly high levels of mercury. This, presumably, resulted from rapid metabolism of the compound and excretion of mercuric ion in the kidney and colon. The net effect was to spare other tissues, and to injure the excretory organs when the dose level was sufficiently high.
PMCID: PMC1319490  PMID: 4248438
17.  Carbamoylation correlates of cyanate neuropathy and cyanide poisoning: relevance to the biomarkers of cassava cyanogenesis and motor system toxicity 
SpringerPlus  2013;2:647.
We sought to elucidate the protein carbamoylation patterns associated with cyanate neuropathy relative to cyanide poisoning. We hypothesized that under a diet deficient in sulfur amino acids (SAA), the carbamoylation pattern associated with cyanide poisoning is similar to that of cyanate neuropathy. Male rats (6–8 weeks old) were fed a diet with all amino acids (AAA) or 75%-deficiency in SAA and treated with 2.5 mg/kg/body weight (bw) NaCN, or 50 mg/kg/bw NaOCN, or 1 μl/g/bw saline, for up to 6 weeks. Albumin and spinal cord proteins were analyzed using liquid chromatography mass spectrometry (LC-MS/MS). Only NaOCN induced motor deficits with significant levels of carbamoylation. At Day 14, we found a diet-treatment interaction effect on albumin carbamoylation (p = 0.07). At Day 28, no effect was attributed to diet (p = 0.71). Mean number of NaCN-carbamoylated sites on albumin was 47.4% higher relative to vehicle (95% CI:16.7-86.4%). Only NaOCN carbamoylated spinal cord proteins, prominently, under SAA-restricted diet. Proteins targets included myelin basic and proteolipid proteins, neurofilament light and glial fibrillary acidic proteins, and 2', 3' cyclic-nucleotide 3'-phosphodiesterase. Under SAA deficiency, chronic but not acute cyanide toxicity may share biomarkers and pathogenetic similarities with cyanate neuropathy. Prevention of carbamoylation may protect against the neuropathic effects of cyanate.
PMCID: PMC3862856  PMID: 24349951
Carbamoylation; Cyanate; Cyanide; Neuropathy; Proteomics
18.  Evaluation, diagnosis, and treatment of lead poisoning in a patient with occupational lead exposure: a case presentation 
Amongst toxic heavy metals, lead ranks as one of the most serious environmental poisons all over the world. Exposure to lead in the home and the workplace results in health hazards to many adults and children causing economic damage, which is due to the lack of awareness of the ill effects of lead. We report the case of a 22 year old man working in an unorganized lead acid battery manufacturing unit, complaining about a longer history of general body ache, lethargy, fatigue, shoulder joint pain, shaking of hands and wrist drop. Patient had blue line at gingivodental junction. Central nervous system (CNS) examination showed having grade 0 power of extensors of right wrist & fingers. Reflexes: Supinator- absent, Triceps- weak and other deep tendon reflexes- normal. Investigations carried out during the admission showed hemoglobin levels of 8.3 g/dl and blood lead level of 128.3 μg/dl. The patient was subjected to chelation therapy, which was accompanied by aggressive environmental intervention and was advised not to return to the same environmental exposure situation. After repeated course of chelation therapy he has shown the signs of improvement and is on follow up presently.
PMCID: PMC2000868  PMID: 17718907
19.  Vitamins: Nutrients, Hormones, Drugs or Poisons? 
Canadian Family Physician  1973;19(11):72-75.
Conventional concepts of daily vitamin requirements may need revision. For example, recent studies on Vitamin C suggest that the recommended daily allowance, while it certainly prevents scurvy, may not saturate the body. Certain disease states and medications raise the daily requirement for specific vitamins. Most claims made by proponents of megavitamin therapy are unproven and without convincing theoretical bases. However, in at least two instances there is enough suggestive evidence to warrant more extensive trials. Although it seems that many vitamins can be given in large doses safely, Vitamins A and D and nicotinic acid, because of their toxicity, must be used with caution.
PMCID: PMC2371213  PMID: 20468999
20.  Deliberate self-poisoning: a study in London casualty departments. 
British Medical Journal  1977;1(6064):805-808.
During a prospective study of the whole spectrum of drug-related problems treated in one month by 62 casualty departments in the Greater London area, 949 cases of deliberate self-poisoning were identified. Nearly three-quarters of the patients were under the age of 40 years and in all age groups women outnumbered men. Psychoactive drugs of some sort were used in 673 incidents (71%) and ordinary analgesics and other drugs were used in 252 (27%). The incidence of polydrug overdose (423; 45%) was much higher than that found in other studies. In at least 256 incidents (27%) there was a history of repeated overdose in the previous 12 months. Comparison with other studies showed a steady decline in the use of barbiturates in deliberate self-poisoning but an increase in the use of non-barbiturate hypnotics, minor tranquilisers, and antidepressants.
PMCID: PMC1606155  PMID: 851739
21.  STUDIES IN LEAD POISONING: Comparison between different Laboratory Tests 
The urinary output of δ-aminolaevulic acid (ALA), coproporphyrins, and lead in 15 leadintoxicated workers was determined and correlated with the degree of intoxication. Raised levels of ALA in the urine show the best agreement with clinical evidence of intoxication.
In addition these values were correlated with the amount of lead excreted after treatment with a total dosage of 9 g. penicillamine. Weak correlations were found between therapeutically excreted lead and initial values for lead and coproporphyrin in urine. In contrast the initial values for ALA correlate very closely (P < 0·001). It is concluded that determinations of the output of ALA are to be preferred in the evalution of lead intoxication and that they point directly to the amount of metabolically active lead in the organism.
PMCID: PMC1069384  PMID: 5836572
22.  The Diagnosis of Industrial Lead Poisoning 
A series of 100 lead workers from different industries, 91 at work and nine admitted to hospital with lead poisoning, was studied in order to define more clearly the clinical and biochemical criteria of lead poisoning in three stages—(A) a presymptomatic state of lead exposure (37 men), (B) a state of mild symptoms or mild anaemia (45 men), and (C) frank lead poisoning with severe symptoms and signs (18 men).
The tests used were haemoglobin, reticulocyte count, and blood lead, and urinary lead, coproporphyrin, δ-aminolaevulinic acid (ALA), and porphobilinogen (PBG) estimations. Of these, the urinary lead was similar for all three groups and the blood lead estimation was of less value for determining the clinical group of the men than the haemoglobin and urinary coproporphyrin or ALA estimations, which correlated well with the clinical assessment and with each other but showed no correlation with the urinary and blood lead levels. PBG levels became raised only with the onset of symptoms of lead poisoning.
A haemoglobin of 13 g./100 ml. (90%) or less is a cautionary sign. Urinary coproporphyrin above 80 μg./100 mg. creatinine (800 μg./litre), ALA above 2·0 mg./100 mg. creatinine (2·0 mg.%), and PBG above 0·15 mg./100 mg. creatinine (0·15 mg.%) were almost always associated with symptoms or signs and were therefore considered to be the upper safety limits. Although the blood lead level does not differentiate between lead toxicity and lead exposure, values above 60 μg. lead/100 g. blood should alert the physician to carry out other tests.
In addition to the above tests, blood pressure, blood urea, and serum uric acid estimations were performed on all the men in order to elucidate the possible role of lead in the production of renal damage. Blood pressure and serum uric acid levels were similar for all three groups but the blood urea level was raised in group C. The reason for this finding was not established.
It was found that scrap metal burning, battery manufacturing, and ship-breaking constituted the gravest lead hazards encountered in this survey whereas wire manufacture constituted the least. Workers in the most modern factory, a car-body pressing plant, gave average values just below the danger levels for the urinary coproporphyrin and ALA estimations despite apparently efficient protective measures. This finding underlines the importance of the medical supervision of lead workers.
PMCID: PMC1008661  PMID: 5642647
23.  Acidaemia and Salicylate Poisoning in Adults 
British Medical Journal  1969;2(5656):547-550.
A review of the arterial acid-base status on admission to hospital of 62 adults with severe salicylate poisoning showed that arterial pH was normal or high in most patients, but low in 8. The mean plasma salicylate concentrations of the acidaemic and nonacidaemic patients were similar and the difference in arterial pH was associated with a marked fall in standard bicarbonate in the former group. No significant difference of Pco2 between the two groups was found, and hence no simple relationship exists between hypocapnia and the development of acidaemia in salicylate poisoning. Acidaemia is shown to be associated with impaired consciousness and to carry a grave prognosis.
PMCID: PMC1983473  PMID: 5769889
24.  Inorganic Phosphate and Sodium Ions Are Cogerminants for Spores of Clostridium perfringens Type A Food Poisoning-Related Isolates▿  
Applied and Environmental Microbiology  2009;75(19):6299-6305.
Clostridium perfringens type A isolates carrying a chromosomal copy of the enterotoxin (cpe) gene are involved in the majority of food poisoning (FP) outbreaks, while type A isolates carrying a plasmid-borne cpe gene are involved in C. perfringens-associated non-food-borne (NFB) gastrointestinal diseases. To cause diseases, C. perfringens spores must germinate and return to active growth. Previously, we showed that only spores of FP isolates were able to germinate with K+ ions. We now found that the spores of the majority of FP isolates, but none of the NFB isolates, germinated with the cogerminants Na+ and inorganic phosphate (NaPi) at a pH of ∼6.0. Spores of gerKA-KC and gerAA mutants germinated to a lesser extent and released less dipicolinic acid (DPA) than did wild-type spores with NaPi. Although gerKB spores germinated to a similar extent as wild-type spores with NaPi, their rate of germination was lower. Similarly, gerO and gerO gerQ mutant spores germinated slower and released less DPA than did wild-type spores with NaPi. In contrast, gerQ spores germinated to a slightly lesser extent than wild-type spores but released all of their DPA during NaPi germination. In sum, this study identified NaPi as a novel nutrient germinant for spores of most FP isolates and provided evidence that proteins encoded by the gerKA-KC operon, gerAA, and gerO are required for NaPi-induced spore germination.
PMCID: PMC2753063  PMID: 19666724
25.  Experimental lead poisoning in the baboon 
Hopkins, A. (1970).Brit. J. industr. Med.,27, 130-140. Experimental lead poisoning in the baboon. Twelve large and three infant baboons were poisoned by the intratracheal injection of lead carbonate in doses ranging from 50 to 135 mg/kg for 39 to 362 days. Eight baboons had one or more epileptic fits. Weakness of the limbs, believed to be of central origin, was seen in three of them. The effect of single and multiple doses of lead on the blood lead is recorded. Anaemia and punctate basophilia were not found. Measurements of nerve conduction velocity, electromyography and histological examination showed no abnormality of the peripheral nerves. The different effects of lead upon different species are discussed.
PMCID: PMC1009086  PMID: 4987891

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