Dose and time effects of combined exposure to lead and ethanol on lead body burden and some neuronal, hepatic and haematopoietic biochemical indices in the rat.

Ethanol (1, 2 or 5 g kg-1) and lead (0.55 g l-1 in drinking water) were given either alone or in combination for 4 months to rats. The uptake of lead in tissues, some lead-sensitive variables, the levels of biogenic amines in different brain regions, hepatic lipid peroxidation, glycogen and blood glucose concentrations were measured. Ethanol or lead when given alone inhibited the activity of blood delta-aminolevulinic acid dehydratase (ALAD). The co-administration of 5 g kg-1 but not 1 or 2 g kg-1 ethanol significantly enhanced the lead-induced inhibition of blood delta-ALAD activity and the elevation of delta-aminolevulinic acid (ALA) excretion. Co-exposure to lead and ethanol (5 g kg-1) produced a more pronounced increase in hepatic lipid peroxidation and blood glucose level than either ethanol or lead alone. This combination also caused a significant increase in the dopamine (DA) contents of striatum, midbrain and pons medulla, norepinephrine (NE) contents in midbrain and 5-hydroxytryptamine (5-HT) contents of hypothalamus, striatum, midbrain and pons medulla over levels produced by lead alone. However, the level of NE in hypothalamus decreased upon co-administration. The uptake and retention of lead was significantly higher in blood, liver, kidney and brain in animals co-exposed to lead and 5 g kg-1 ethanol. Blood and kidney lead was also increased by 2 g kg-1 ethanol. The results suggest that prolonged and heavy consumption of alcohol may increase the toxicity of lead.