Changes in neurotransmitter receptors and neurobehavioral variables in rats co-exposed to lead and ethanol

The influence of lead (10 mg/kg) and ethanol (10% v/v, in drinking water) administration, either alone or in combination for 8 weeks was investigated on the uptake of lead in tissues, dopamine, benzodiazepine and cholinergic (muscarinic) receptors, motor activity, number of fighting episodes and several selected lead-sensitive biochemical indices in young rats. Lead or ethanol treatment did not elicit any appreciable influence on body weight gain, tissue weight, and food intake. However, a decreased amount of mean water intake was noticed in animals ingesting ethanol plus lead. Both lead and ethanol when administered individually exacerbate the decrease of blood delta-aminolevulinic acid dehydratase (ALAD) activity while lead and ethanol administered together exhibited a pronounced inhibition of ALAD activity. A significant increase in hepatic GSH levels, hepatic and brain MDA levels was also observed in animals co-exposed to lead and ethanol compared to lead alone treated rats. Simultaneous exposure to lead and ethanol also resulted in a significantly more pronounced decrease in binding of [3H]fluintrazepam in membranes prepared from the fronto-cortical region compared to the corresponding controls. The binding of [3H]spiroperidol to striatal and [3H]quinuclidinyl benzylate (QNB) to cerebellar membranes remained unaltered in all the exposed animals. Spontaneous locomotor activity and aggressive behaviour increased significantly in the group treated with both lead and ethanol compared to the control group. The lead concentrations in blood, liver, kidney and brain were significantly higher in rats exposed simultaneously to lead and ethanol compared to lead alone exposed group. The results indicate more pronounced neurotoxic and neurobehavioural changes in animals co-exposed to lead and ethanol; however, the exact mechanism or site of its action is still not clear.