Histopathological evidence confirmed the protection offered by lutein from the tissue damage caused by hepatotoxins. The hepatoprotective action may be due to lutein's ability to scavenge reactive oxygen radicals.

Background: Carotenoid lutein was evaluated for antiulcerogenic activity in rats. Methods: Gastric ulcer was induced in fasted rats by oral administration of ethanol (95%) (5 mL/kg body weight). Lutein (100 and 250 mg/kg body weight) was administered everyday for 5 days prior to alcohol administration. Results: The ulcer index which is a measure of the severity of ulcers was found to be reduced in lutein-treated groups. Morphological and histopathological examination supported the protection of lutein during alcohol-induced damage in rat stomach. Antioxidant enzymes, such as catalase, super oxide dismutase, glutathione peroxidase as well as glutathione levels, which were found to be reduced in the gastric mucosa of alcohol-treated groups, were found to be elevated after lutein treatment. Conclusions: The mechanism of antiulcer activity may be due to the inhibition of oxidative stress produced by alcohol by lutein administration. These findings suggest the potential therapeutic use of lutein as an effective antiulcer agent.

Cisplatin is one of the most potent anticancer drugs available for the treatment of a variety of tumors. One of the side effects of this drug is nephrotoxicity. Current research evidence indicates that the renal toxicity is mainly due to the reactive oxygen molecules generated by cisplatin. In the present study, we evaluated the nephroprotective activity of lutein, a non-toxic carotenoid with strong antioxidant activity, to reduce cisplatin-induced renal damage in mice. Serum urea and creatinine levels in the cisplatin-induced mice were significantly elevated compared to those of the control group, and nephrotoxicity was reduced by the lutein treatments (P<0.01). In the cisplatin-treated control group as well as in the vehicle control group, antioxidant enzymes in the kidney, such as superoxide dismutase, as well as catalase activity and level of reduced glutathione were reduced, and the level of malondialdehyde was elevated. Antioxidant enzymes were significantly increased by lutein treatment, and the level of malondialdehyde declined significantly in lutien-treated mice. White blood cell count and bone marrow cellularity, which were significantly reduced in the cisplatin-treated group, were also significantly elevated in all lutein-treated groups (P<0.001). The results of the study show that lutein effectively protected the kidneys of mice treated with cisplatin; these results are also supported by the histopathologies of the kidney tissues of treated mice.

We set out to determine the effect of oxycarotenoid lutein on reducing cardiac and renal toxicity induced by doxorubicin (DXR). We started with oral administration in rats of lutein for 15 d before administering DXR (30 mg/kg body weight, intraperitoneally, in a single dose). Animals in all groups were sacrificed 24 h after DXR administration. Serum markers of cardiac injury lactate dehydrogenase, creatine phosphokinase, serum glutamate oxaloacetate transaminase, and serum glutamate pyruvate transaminase increased drastically after DXR but decreased after lutein treatment (p < 0.001). Elevated serum urea and creatinine in DXR-treated rats were reduced by lutein treatment (p < 0.001). Lutein increased superoxide dismutase, catalase, glutathione peroxidase, and glutathione levels in cardiac and renal tissues of DXR-treated rats. Pretreatment of lutein reduced DXR-induced rise of oxidative stress markers including lipid peroxidation, tissue hydroperoxides, and conjugated dienes in cardiac and renal tissue. These findings were supported by electrocardiogram measurements and histopathological analyses. Results confirmed the protection of lutein against cardiac and renal toxicity induced by DXR in rats.

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