Glutathione transferase mu deficiency is not a marker for predisposition to sulphonamide toxicity.
Glutathione transferase mu activity, a marker for susceptibility to lung cancer and chemically induced cytogenetic damage, is not a predictive index for the predisposition to sulphonamide hypersensitivity reactions. However, considering the functional diversity and broad, overlapping substrate specificity of GSH-dependent enzymes, it is conceivable that an as yet unidentified deficiency in another GST isozyme or GSH-related enzyme may be a marker for sulphonamide toxicity. In addition, heterogeneity in cellular repair mechanisms and the diversity of the human immune response [22] may also contribute to the manifestation of the toxic effects of sulphonamides. Experiments are currently in progress to determine which of this myriad of variables is predominantly responsible for inter-individual susceptibility to the idiosyncratic reactions produced by these antibacterial agents.
Riley
R J
RJ
Division of Clinical Pharmacology and Toxicology, Hospital for Sick Children, Toronto, Canada.
Cribb
A E
AE
Spielberg
S P
SP
D000293:Adolescent; D000328:Adult; D002470:Cell Survival / Q000187:drug effects; D002648:Child; D002675:Child, Preschool; D004198:Disease Susceptibility; D004353:Drug Evaluation, Preclinical; D004342:Drug Hypersensitivity / Q000097:blood / Q000209:etiology*; D005982:Glutathione Transferase / Q000097:blood* / Q000235:genetics; D006801:Humans; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects* / Q000201:enzymology; D013420:Sulfamethoxazole / Q000494:pharmacology*; D013449:Sulfonamides / Q000009:adverse effects*
D013449:Sulfonamides; D005982:Glutathione Transferase; D013420:Sulfamethoxazole