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Effect of Three Chlorinated Pesticides on hsrω Stress gene in Transgenic Drosophila melanogaster

Expression of hsrω stress gene in the third‐instar larvae of 951‐lacZ2 (hsrω‐lacZ having–844pb sequence) and 498‐lacZ1 (hrsω‐lacZ having –498bp sequence) strains of Drosophila melanogaster at LC50 and lower dietary concentrations of hexachlorocyclohexane (HCH) pentachlorophenol (PCP), and endosulfan was examined in relation to larval mortality by β galactosidase activity, vital dye staining, and salivary gland polytene chromosome puffing. Our results showed that both HCH and PCP at lower concentrations evoked strong hsrω stress gene expression in the larval tissues while endosulfan did not. On the other hand, puffing data revealed that endosulfan at lower doses, induced well‐developed puff at the resident site (93D) of the hsrω gene but the transgenic sites (30B in 951‐lacZ2 and 44B in 498‐lacZ1 strain) did not show any well‐developed puff. Regression in hsrω stress gene expression in 951‐lacZ2 strain at LC50 concentrations of HCH and PCP after 48 h was concurrent with extensive tissue damage as evident by trypan blue staining. Similarly, strong hsrω expression was accompanied by insignificant trypan blue staining in the larval tissues of this strain after shorter duration of exposure (2–12 h) to these toxicants. Although endosulfan under similar experimental condition did not induce hsrω, strong trypan blue staining indicated extensive tissue damage after 48 h of exposure. The present study suggests that all the three toxicants pose cytotoxic potential to Drosophila. While protective role of this stress gene was evident at the initial stages of exposure, extensive tissue damage in the later stages of intoxication accompanied by autorepression of hsrω led to larval mortality. The study further suggests that –844bp upstream sequence of the gene is adequate for hsrω inducibility against HCH and PCP but not for endosulfan for which responsive elements may be searched further upstream. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:173–186, 2001