Aluminium administration is associated with enhanced hepatic oxidant stress that may be offset by dietary vitamin E in the rat

Abstract

It has been proposed that aluminium toxicity may be mediated, at least in part, by free radical generation. We have investigated the effects of aluminium lactate administration on indices of hepatic oxidant stress, and the consequences of concomitant dietary vitamin E, in male albino Wistar rats. Aluminium lactate was administered for 4 weeks, by ip injection at 10 mg aluminium/kg body weight. Groups of animals received a chow diet containing 0, 5, 15, or 20 mg vitamin E/g of food. A control group of rats received a normal chow diet, without being injected with aluminium. The rats were killed after 4 weeks, and blood and liver tissue removed for the measurement of aluminium and markers of oxidative stress. Plasma and liver aluminium levels were increased in all groups of animals receiving aluminium lactate (P < 0.01), although these levels were significantly reduced in rats receiving concomitant vitamin E (P < 0.05). Aluminium treatment was associated with significantly increased levels of hepatic reactive oxygen species (ROS) (P < 0.01) that were attenuated by concomitant vitamin E (P < 0.05). Hepatic catalase and reduced glutathione levels were both reduced in animals treated with aluminium (P < 0.05).

Figure 1

Aluminium level in different treatment groups. a– Plasma. b– Liver tissue. Values are means ± SEM for n = 5. *P < 0.001 compared to control; ⁺P < 0.01 compared to Al alone.

Figure 2

Plasma Vitamin E levels in different treatment groups. Values are means ± SEM for n = 5. *P < 0.001 compared to control; ⁺P < 0.01 compared to Al alone.

Figure 3

Liver characteristics in different treatment groups. a – ROS production. b – GSH content. c – catalase activity. Values are means ± SEM for n = 5. *p < 0.001 compared to control; ⁺p < 0.01 compared to Al alone.