Neurobehavioural and neurotoxic effects of L-ascorbic acid and L-tryptophan in lead exposed rats

Lead is an environmental toxicant, occupational and environmental exposures remain a serious problem in developing and industrializing countries.

This study is designed to investigate the effects of L-ascorbic acid and L-tryptophan on the neurotoxicity and neurobehavioural alterations in lead exposed male Sprague Dawley rats.

Experimental animals were exposed to oral doses of lead (Pb), L-ascorbic acid, and L-tryptophan at 75 mg/kg body weight, 40 mg/kg body weight, and 20 mg/kg body weight respectively, while control animals received 0.90% saline solution. Oral administration spanned for four weeks after which changes in neuro-behaviour, organ weight, blood deposition of Pb, brain serotonin, tryptophan and neuronal redox status were determined. Changes in organ weight, blood lead levels, neuro-behavioural characteristics, brain serotonin and tryptophan contents, and brain redox status were determined.

The results indicated that Pb exposure increased blood lead, organ-weight index, and behavioural signs of anxiety and aggression. The sub-chronic exposure to Pb also decreased brain serotonin, while causing oxidative stress by decreasing reduced glutathione levels, antioxidant enzyme activity and increasing lipid peroxidation and brain protein contents. L-ascorbic acid attenuated both Pb induced neuronal oxidative stress, and abnormalities in behaviour. But L-tryptophan ameliorated Pb altered neurobehaviour with no significant effect on Pb induced oxidative stress in the brain. Co-administration of L-ascorbic acid and L-tryptophan on Pb exposed rats showed a reversal in all indices assessed towards the physiological state of control.

This suggests that L-ascorbic and L-tryptophan can be used to compliment chelating therapy in lead neurotoxicity.