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ABSTRACT:This study aimed at investigating the efficacy of vitamins (C and E), selenium and silymarin (an antioxidant complex from Silybum marianum) supplementation in reducing toxic effects of ethanol on liver weight and some blood parameters. Sixty male rabbits, individually housed in steel cages, were randomly divided into three groups. The first was a control group, the second received balanced diet and daily 20% (v/ v) ethyl alcohol in their drinking water, the third received the same diet and 20% (v/v) ethanol in their drinking water and treated with vitamin C (1 mg/100 g body weight, BW), vitamin E (1 mg/100 g BW), selenium (0.01 mg/ 100 g BW) and silymarin (1 mg/100 g body weight) by gastric tube daily. Five animals per group were slaughtered every two weeks and liver and blood samples were taken after 2, 4, 6 and 8 weeks of treatment. Ethanol decreased body weight of rabbits and induced hepatomegally and apoptotic DNA fragmentation in hepatocytes. Chronic alcohol consumption induced significant increases in serum glucose, triglycerides and cholesterol levels whereas serum total protein content decreased. Significant increases in serum ALT, AST, ALP and LDH activities were observed in ethanol-treated rabbits. The treatment of alcohol-abused animals with vitamins (C and E), selenium and silymarin enhanced significant improvement in the biochemical, physiological and molecular aspects indicating their protective effects against alcohol toxicity.

This study investigated the protective role of lactoferrin (LF) against lead acetate poisoning in female albino rats (Rattus norvegicus). Four equal groups of animals (6 rats/group) were treated orally/daily by gastric tube for eight weeks. The first group was the control group, the second group received LF (10 mg/kg of body weight), the third group received lead acetate (100 mg/kg of body weight), and the fourth group received both LF and lead acetate with the same doses. After eight weeks, blood and tissue samples were taken for hematological, biochemical and histological analyses. The results showed that lead exposure induced significant elevations (P<0.05) in the activity of plasma alanine aminotransferase and aspartate aminotransferase, plasma creatinine concentration, plasma lead level, hepatic cytochrome P450, and the brain malondialdehyde. Brain superoxide dismutase activity was reduced significantly (P<0.05), in response to the lead toxicity. Lead acetate caused many pathological changes in the liver, brain, and kidneys tissues. Severe DNA fragmentation in the brain tissue was observed after lead treatment. On the other hand, LF was found to modulate significantly (P<0.05) the deteriorations in most parameters under investigation. In conclusion, these data suggest that LF has a protective function in the molecular and histological processes causing neurodegeneration, as well as renal and hepatocyte injury induced by lead.