Protective Effect of Opuntia dillenii Haw Fruit against Lead Acetate-Induced Hepatotoxicity: In Vitro and In Vivo Studies.

Lead is one of the most common environmental contaminants in the Earth's crust, which induces a wide range of humans biochemical changes. Previous studies showed that Opuntia dillenii (OD) fruit possesses several antioxidant and anti-inflammatory properties. The present study evaluates OD fruit hydroalcoholic extract (OHAE) hepatoprotective effects against lead acetate- (Pb-) induced toxicity in both animal and cellular models. Male rats were grouped as follows: control, Pb (25 mg/kg/d i.p.), and groups 3 and 4 received OHAE at 100 and 200 mg/kg/d + Pb (25 mg/kg/d i.p.), for ten days of the experiment. Thereafter, we evaluated the levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), catalase (CAT) activity and malondialdehyde (MDA) in serum, and liver histopathology. Additionally, the cell study was also done using the HepG2 cell line for measuring the direct effects of the extract on cell viability, oxidative stress MDA, and glutathione (GSH) and inflammation tumor necrosis factor-α (TNF-α) following the Pb-induced cytotoxicity. Pb significantly increased the serum levels of ALT, AST, ALP, and MDA and liver histopathological scores but notably decreased CAT activity compared to the control group (p < 0.001 for all cases). OHAE (100 and 200 mg/kg) significantly reduced the levels of serum liver enzyme activities and MDA as well as histopathological scores while it significantly increased CAT activity compared to the Pb group (p < 0.001-0.05 for all cases). OHAE (20, 40, and 80 µg/ml) concentration dependently and significantly reduced the levels of MDA and TNF-α, while it increased the levels of GSH and cell viability in comparison to the Pb group (p < 0.001-0.05 for all cases). These data suggest that OHAE may have hepatoprotective effects against Pb-induced liver toxicity both in vitro and in vivo by its antioxidant and anti-inflammatory activities.

Oxidative stress and hepatic injury induced in mice fed a Sarcocystis hirsuta cyst extract.

We studied the toxic effects of a Sarcocystis hirsuta cyst extract fed to mice. Degenerative changes were found in mice gavage-fed fresh, frozen, and heat-treated S. hirsuta cyst extract. There were increases in the levels of serum aspartate aminotransferase and alanine aminotransferase as well as hepatic and brain malondialdehyde (MDA) levels along with concomitant decreases in catalase (CAT) and superoxide dismutase (SOD) activities of mice receiving fresh and frozen S. hirsuta extracts. Gavage feeding of heat-treated S. hirsuta cyst extract had no effects on liver enzymes or brain MDA content, but the liver MDA level did increase. Mice in the heat-treated cyst group showed reduced CAT and SOD activities as well as increased hepatic MDA levels compared to those in the control group. These results indicate that an extract of S. hirsuta cyst can induce oxidative stress and hepatic injury, even after heat treatment.