Benzo[a]pyrene and Benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide induced locomotor and reproductive senescence and altered biochemical parameters of oxidative damage in Canton-S Drosophila melanogaster

[Display omitted] •Canton-S strain of Drosophila melanogaster was investigated as a possible experimental model of Benzo[a]pyrene (B[a]P) toxicity.•B[a]P and its metabolite, BPDE, caused significant changes in negative geotaxis, fecundity and biochemical parameters of toxicity of the flies.•The compounds interacted with Drosophila glutathione-S-transferase (GST) and acetylcholinesterase (AChE) in a molecular docking analysis.•BPDE induced a high rate of mortality in this strain of flies possibly through AChE inhibition.•Canton-S strain of Drosophila melanogaster could be an alternative model to study B[a]P toxicity. Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon (PAH) commonly found in cigarette smoke, automobile exhaust fumes, grilled meat, and smoked food among others. Exposure to B[a]P is associated with a range of toxic effects including developmental, neurological, oxidative, inflammatory, mutagenic, carcinogenic and mortal. Efficient and more affordable experimental models like Drosophila melanogaster could provide more insight into the mechanism of PAH toxicity and help develop new strategies for prevention, diagnosis and treatment of PAH-related conditions. In this study, we examined the induction of some biochemical changes along with mortality and functional senescence by B[a]P and its metabolite, benzo[a]pyrene- 7,8-dihydrodiol-910-epoxide (BPDE) in the Canton-S strain of Drosophila melanogaster, with the aim to establish an alternative assay medium for B[a]P toxicity in flies. Flies were exposed to 2–200 μM of B[a]P and 1–10 μM of BPDE through diet for a seven-day survival assay followed by a four-day treatment to determine the effects of the compounds on negative geotaxis, fecundity and some biochemical parameters of oxidative damage. BPDE significantly reduced the survival rate of flies along the 7 days of exposure whereas B[a]P did not cause any significant change in the survival rate of flies. B[a]P and BPDE significantly reduced the climbing ability of flies after 4 days of exposure. Rate of emergence of flies significantly reduced at 10–200 μM of B[a]P and 5–10 μM of BPDE. Both compounds caused various levels of alterations in the values of reduced glutathione (GSH), total thiol (TSH), glutathione-S-transferase (GST), catalase (CAT), hydrogen peroxide (H2O2), nitric oxide (NO) and acetylcholinesterase (AChE) of the flies. The compounds also exhibited high binding affinities and molecular interactions with the active site amin