[Evaluation of porphyrinogenic effect of lindane in rats]

In order to study the porphyrinogenic ability of lindane in mammals, rats were treated with the pesticide suspended with the aid of Tween or dissolved in oil during about 3 months. The urinary excretion of porphyrins and its precursors: delta-aminolaevulinate (ALA) and porphobilinogen (PBG), as well as the faecal excretion of coproporphyrin (COPRO) and protoporphyrin (PROTO) was determined weekly. At the end of the treatment the hepatic activities of ALA Synthase (ALA-S), the first and rate limiting enzyme of haem pathway, and porphyrinogen carboxy-lyase (PCL), enzyme which sequentially decarboxylates uroporphyrinogen (8 COOH) to coproporphyrinogen (4 COOH), were assayed. Lindane moderately increased the urinary excretion of porphyrins and its precursors, being the former the mainly affected parameter. The faecal excretion of COPRO and PROTO was also increased. However, the hepatic activity of ALA-S was not altered. This would suggest that the regulatory haem pool was not affected. Nor was PCL activity altered in spite of being the key enzyme for the attack of other chlorinated compounds. Although hexachlorobenzene (HCB), a very well known porphyrinogenic drug, and lindane are chemically related and generate similar metabolites, the last one produces a small and qualitatively different alteration of haem biosynthesis. This may be related with the absence or scarce formation of the reactive metabolite that accounts for the porphyrinogenic ability of HCB.