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Polyphenol-rich dietary foodstuffs, consumed as an integral part of vegetables, fruits, and beverages have attracted attention due to their antioxidant and anticancer properties. Ellagic acid (EA), a polyphenolic compound widely distributed in fruits and nuts, has been reported to scavenge free radicals and inhibit lipid peroxidation. Chronic consumption of alcohol potentially results in serious illness including hepatitis, fatty liver, hypertriglyceridemia, and cirrhosis. A little is known about the influence of EA on alcohol toxicity in vivo. Accordingly, in the present study, we have evaluated the protective effects of EA on lipid peroxidation and lipid levels during alcohol-induced toxicity in experimental rats. Forty female albino Wistar rats, which were weighing between 150-170 g were used for the study. The toxicity was induced by administration of 20% alcohol orally (7.9 g/kg body wt.) for 45 days. Rats were treated with EA at three different doses (30, 60, and 90 mg/kg body wt.) via intragastric intubations together with alcohol. At the end of experimental duration, liver marker enzymes (i.e., aspartate transaminase, alanine transaminase), lipid peroxidative indices (i.e., thiobarbituriacid reactive substances and hydroperoxides) in plasma, and lipid levels (i.e., cholesterol, free fatty acids, triglycerides and phospholipids) in tissues were analyzed to evaluate the antiperoxidative and antilipidemic effects of EA. Liver marker enzymes, lipid peroxidative indices, and lipid levels, i.e., cholesterol, triglycerides and free fatty acids, were significantly increased whereas phospholipid levels were significantly decreased in the alcohol-administered group. EA treatment resulted in positive modulation of marker enzymes, peroxidative indices, and lipid levels. EA at the dose of 60 mg/kg body wt. was found to be more effective when compared to the other two doses. Histological changes observed were also inconsistent with the biochemical parameters. Our study suggests that EA exerts beneficial effects at the dosage of 60 mg/kg body wt. against alcohol-induced damage, and it can be used as a potential drug for the treatment of alcohol-abuse ailments in the near future.

In the present study, ferulic acid (FA), a naturally occurring nutritional compound, was investigated for its protective effect against nicotine-induced toxicity in a dose dependent manner. The toxicity was induced by subcutaneous injection of nicotine at a dose of 2.5 mg/kg body weight (b.w.) for 22 weeks in female albino Wister rats. Simultaneously, rats were treated with FA at three different doses (10, 20 and 40 mg/kg b.w.) via intragastric intubations for 22 weeks. At the end of the experiment, circulatory marker enzymes (i.e. lactate dehydrogenase and alkaline phosphatase) and tissue (lung, liver and kidney) lipid levels (i.e. cholesterol, free fatty acids, triglycerides and phospholipids) were analysed, which were significantly increased in the nicotine-treated group, whereas FA treatment positively modulated these levels. FA at a dose of 20 mg/kg b.w. was found to be more effective when compared with the other two doses. The lung, liver and kidney excised from the different groups were fixed and stained to perform histological assessments. The protective effect of FA on histological observations confirms that 20 mg/kg b.w. of FA modulates the deleterious effects of nicotine. The results suggest that FA exerts its inhibitory action against nicotine-induced tissue damage through its antioxidant and antihyperlipidemic properties.

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