AbstractRats were exposed to 300 ppmm‐xylene vapour for 1 or 2 weeks, 6 h daily, 5 days a week. One group was simultaneously given disulfiram in the drinking water (53 μmol kg−1, daily). The disulfiram treatment inhibited propionaldehyde dehydrogenase; such inhibition did not occur whenm‐methylbenzaldehyde (i.e., the aldehyde ofm‐xylene metabolism) was used as the substrate. Gastric gavage with higher drug doses (0.5 g kg−1, administered one or three times) confirmed this finding. Intermittent inhalation exposure tom‐xylene for 2 weeks lowered the non‐protein sulphhydryl group content in liver and increased the activities of microsomal NADPH‐cytochromecreductase, 7‐ethoxycoumarinO‐deethylase and UDP‐glucuronosyltransferase in liver. Concomitantly, the oxidation ofm‐xylenein vitrowas also enhanced. Combined exposure to the solvent and the drug somewhat inhibited the increases in the hepatic drug metabolism and in the rate of microsomal xylene oxidationin vitrowhichm‐xylene had induced, whereas the renal drug metabolism remained almost unaffected. Despite the changes in the monooxygenase, the solvent burden in the perirenal fat remained comparable. The significance of impaired aldehyde metabolism inm‐xylene toxicity could not be confirmed in male Wistar rats
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