Protection of extract from leaves of Ardisia compressa against benomyl-induced cytotoxicity and genotoxicity in cultured rat hepatocytes.

The potential of the Ardisia compressa extract (EA) was examined regarding its capacity to reduce the cytotoxic effect of benomyl on rat hepatocytes. The protective effect was evaluated by Janus Green dye exclusion method. An approximate 50% cytotoxic effect of benomyl on hepatocytes was observed at 35mug/ml after 2hr of incubation. (-)Epigallocatechin 3-gallato (EGCG) and EA decreased the viability of hepatocytes at concentrations above 3mug/ml and 2.52mug, equivalent to (+)catechin/ml, respectively. A protective effect against benomyl was observed when hepatocytes were previously exposed to EGCG (3mug/ml) or EA (2.52mug, equivalent to (+)catechin/ml) followed by incubation with benomyl (35mug/ml) alone. When EGCG or EA were in contact with cells, either simultaneously or after pretreatment with benomyl, did not protect hepatocytes. EGCG (1.3x10(-2)mug/ml) or EA (9.8x10(-2)mug, equivalent to (+)catechin/ml) inhibited 57% and 34%, respectively, the unscheduled DNA synthesis (UDS) induced by benomyl at a concentration of 23x10(-2)mum, when both were incubated with hepatocytes prior to benomyl. The simultaneous incubation of benomyl with EGCG or EA did not protect the cell against the genotoxic effect of benomyl. These results indicate that the dried leaves extract of Ardisia compressa protect rat hepatocytes from benomyl-induced cytotoxicity and genotoxicity.

Effect of carotenoids against genotoxicity of diethylnitrosamine on rat hepatocytes.

Carotenoids have been considered as special nutrients due to their biological activity as provitamin A compounds, and because of their natural antioxidant and anticarcinogenic properties. The main objective of this study was to evaluate the protective effect of carotenoids against the genotoxic cellular damage induced by diethylnitrosamine (DEN), a potent hepatocarcinogen. Normal and freshly isolated hepatocytes were cultured as the biological system. Concentrations of 2.5 and 5 mum DEN caused 1.3 and 2.0 times more DNA T(3)H incorporation, respectively, when compared with control cells. Pure carotenoids, beta-carotene (50 mum), lutein (1 mum) and a carotenoid extract from green peppers (1 mum eq. lutein) were used as functional nutrients to protect the cells. All the carotenoids studied prevented the genotoxic damage caused by 2.5 mum DEN. When 5 mum DEN was used, only beta-carotene and the pepper extract inhibited the damage up to 30-40%. Carotenoids provide a dose-dependent protective effect against DNA damage induced by DEN in isolated hepatocytes.