In the present study, rabbits have not presented signs of toxicity in all the experimental period. The animals of PLFO group have exhibited a normal behavior in comparison to CRL group. Any macroscopically lesions were observed in rectal mucosa. No significant differences were observed in body weight gain of the two groups. In view of these partial results, we can assert that PLFO did not cause clinical alterations for rabbits during its application for 6 consecutive weeks.
In several organs, cell damage is followed by released of a number of cytoplasmic enzymes to the blood, phenomena that provides the basis for clinical diagnosis (Sundberg et al., 1994
). In our study, hepatic function was evaluated by measuring plasma ALT and AST activities, albumin and total proteins concentrations. Renal function was evaluated by measuring plasma creatinine and urea concentrations (Davis and Berdt, 1994
; Finco, 1997
; Correges et al., 1998
). Regarding biochemical data, all biochemical blood parameters investigated in this study were within the physiological range as reported by Archetti et al. (2008)
. Additionally, our results showed a significant decrease of transaminases; AST and ALT concentrations were 1.8 and 2.4 times respectively lower than those observed in the control group. It is known that damage to the structural intergrity of liver is reflected by increase in the liver hepato-specific enzymes (ALP, ALT and AST) in the serum, because they are cytoplasmic in location and are released into circulation after cellular damage (Janbaz and Gilani, 1995
; Venkateswaran et al., 1995
). These transaminases play important roles in amino acids metabolism and providing necessary intermediates in gluconeogenesis (Hanley et al., 1986
). According to this, the significant decrease of plasma transaminases (ALT and AST) activities of treated rabbits could indicate an improvement in liver function due to a possible hepatoprotective activity of PLFO. This pharmacological property has been investigated in Pistacia lentiscus
plant in earlier study. It has been reported by Janakat and Al-Merie (2002) that aqueous extract of P. lentiscus
(both boiled and non-boiled) showed marked antihepatotoxic activity against CCL4
(Carbon tetrachloride) by reducing the activity of the three enzymes (ALP, ALT and AST) and the level of bilirubin. They concluded that P. lentiscus
is effective in the treatment of hepatic jaundice in the rat.
According to literature, the hepatoprotective medicinal preparations must: possess antioxidant properties; stabilize cell membranes; inhibit microsomal cytochrome P-450-dependent system activity, as the primary source of oxygen free radicals, and have anti-inflammatory properties (Lukivskaya et al. 2006
). Its worth asking whether compounds of PLFO were implicated in the amelioration of liver functions. Preliminary studies indicated that this fatty oil contains two fractions: the unsaponifiable fraction presented mainly by tocopherols and phytosterols; the saponifiable fraction which is rich in unsaturated fatty acids (UFA) and saturated fatty acids (SFA). Phytosterols have been found to exhibit anti-inflammatory and anti-oxidant activities (Moreno, 2003
). Tayal et al. (2007)
reported that alpha-tocopherol (Vitamin E) is a potent antioxidant that provides hepatoprotection by scavenging free radicals. Hernández et al. (2005)
reported that treatment with a balanced diet rich in olive oil contributed to the recovery of the liver from hepatic steatosis, by decreasing activation of hepatic stellate cells by MUFAs, which are less susceptible to lipid peroxidation compared to PUFAs. Moreover, previous studies carried out in fibrotic rats showed that olive oil, in contrast to polyunsaturated oils, could protect against the development of fibrosis (Szende et al., 1994
). In view of these cited studies, the variations of transaminases in PLFO group may be essentially due to tocopherols, phytosterols and unsaturated fatty acids compounds.
Fasting glucose level was found to be increased (21.3%) in PLFO group compared to value of untreated rabbits. Values in the two groups were correspondent to standards. It is known that liver is the main organ of glycogen metabolism. The decrease of glycogen in liver is a common result of hepatic insufficiency after liver lesions caused by toxic compounds. This hepatic insufficiency can cause an increase of insulin in blood, and a consecutive reduction of the blood sugar content, which is consistent with glycogen/glucose level in liver (Wu et al., 2005
). In our study, elevation of glucose level may be explained by an effect of PLFO on liver cell metabolism. This later may affect directly the synthesis, the storage and the decomposition of glycogen in liver. In addition, this fatty oil was known for its antioxidant properties due to tocopherols and phytosterols. The inhibition of fatty acids oxidation can lead to a decrease in glycogenesis due to the inhibition of acetyl CoA (Golden and Kean, 1984
Regarding renal function, variations of creatinine and urea were found to be none significant between the two groups; consecutively renal function was not alliterated by PLFO treatments. Decreases in concentration of whole plasma proteins and albumin have been proposed as indicators of the alteration of protein synthesis (Kubena et al., 1993
). A drop in serum albumin level is usually the result of decreased protein synthesis by the liver or increased protein loss trough the gut of the kidney, other possible cause of decrease in albumin may include mal absorption (Orhue et al., 2005
). In the present study, total proteins and albumin were reduced very slightly and none significantly in tested group. This is why we report that PLFO treatment had no significant impact on proteins and albumin concentrations.