The activity of alanine transaminase (ALT; IU/l) in group 1 was 19.346 ± 0.131, which was significantly (P<0.05) increased in Cd toxic control groups 2, 6, 7 and 8 to 60.279 ± 0.166, 60.115 ± 0.022, 59.728 ± 0.208 and 60.030 ± 0.080, respectively, at the end of 4th wk. In groups, 6, 7 and 8 following treatment, the activity was significantly (P</0.05) reduced to 41.743 ± 0.331, 42.075 ± 0.056 and 40.023 ± 0.088, respectively, as compared to their respective 4th wk values and that of group 2 (68.071 ± 0.012) at the end of 6th wk.
The activity of alkaline phosphatase (ALP; units/ml) in group 1 was 70.785 ± 0.620, which was significantly (P<0.05) increased in the Cd toxic control groups 2, 6, 7 and 8 to 80.211 ± 1.149, 78.674 ± 0.515, 78.206 ± 0.337 and 78.161 ± 0.314, respectively, at the end of 4th wk. In groups 6, 7 and 8 following treatment, the ALP activity was significantly (P<0.05) decreased (72.034 ± 0.065, 70.061 ± 0.198 and 70.04 ± 0.012, respectively) when compared to their respective 4th wk values and that of group 2 (82.693 ±0.216) at the end of 6th wk.
The activities of ALT and ALP are elevated following hepatocellular injury.[4
] Demerdesh et al
] reported an increase in the activity of ALT and ALP in plasma, when rats were fed with Cd at 5 mg/kg. Treatment with E. officinalis
, vitamin E and stressroak following discontinuation of cadmium resulted in a significant reduction in the activity of ALT. The hepatocellular injury due to cadmium could be attributed to the cadmium-induced generation of free radicals and the reversal of the findings following treatment could be attributed to the antioxidant and the hepatoprotective potential of the drugs in test. Alcoholic and aqueous extracts of the fruits of Emblica
have shown hepatoprotective properties in experiments in rats; it inhibited hepatic lipid peroxidation and the increase of serum levels of ALT, aspartate transaminase (AST) and lactate dehydrogenase (LDH). These results support the use of Emblica
fruit for hepatoprotection.[6
] However, simultaneous supplementation of drugs in the test along with cadmium revealed a significant increase in ALT and ALP activities at different time intervals when compared to the plain basal diet control, but the values were significantly lower in comparison to pure cadmium toxic control group 2. This finding suggests the prophylactic potential of these drugs to prevent cadmium-induced toxic manifestations, though there was no complete prevention of changes.
The renal indices such as serum urea and creatinine were significantly (P
<0.05) increased in toxic controls 2, 6, 7 and 8 at the end of 4th
wk when compared to group 1 . This could be due to the oxidative damage of cadmium on renal tissue. However, in groups 6, 7 and 8 following treatment with E. officinalis
, vitamin E and polyherbal formulation, respectively, the renal profile revived to normal, at the end of 6th
wk, suggesting the involvement of oxidative damage prior to treatment. Non-protein nitrogenous (NPN) substances such as serum urea and creatinine are increased only when renal function is below 30% of its original capacity in birds. Plasma urea appears to be the single most useful variable for detection of pre-renal causes of renal failure.[4
] In the present study, the serum urea and creatinine levels were significantly increased in toxic controls at the end of 4th
wk as compared to the remaining groups. The nephrotoxic metal cadmium at micromolar concentrations induces apoptosis of rat kidney proximal tubule (PT) cells within 3-6 hours of exposure. This involves a complex and sensitive interplay of signaling cascades involving mitochondrial pro-apoptotic factors, calpains and caspases, whose activation is determined by cadmium concentration and the duration of cadmium exposure.[7
] Cadmium-induced apoptosis in rat kidney epithelial cells involves decrease in nuclear factor-kB (NF-kB) activity.[8
] Treatment in groups 6, 7 and 8 with E. officinalis
, vitamin E and stressroak, respectively, following discontinuation of cadmium, resulted in significant decrease in serum creatinine and blood urea nitrogen (BUN) as compared to Cd toxic control group 2, which suggests their protective role. However, simultaneous supplementation of drugs in test along with cadmium revealed a significant increase in serum creatinine and BUN at different time intervals when compared to basal diet control, though the values were significantly lower in comparison to pure cadmium toxic control group 2. This finding suggests the prophylactic potential of these drugs to prevent cadmium-induced toxic manifestations, though there was no complete prevention of the changes. The beneficial renal protective actions of drugs in test may be attributed to their antioxidant/free radical scavenging actions and protection of protein thiols from deleterious actions of cadmium in kidney.
In conclusion, the study revealed that cadmium has the potential to induce hepatotoxicity and nephrotoxicity and supplementation with E. officinalis, vitamin E and polyherbal formulation (stressroak) has a beneficial role in preventing the adverse effects.