Journal
INHALATION TOXICOLOGY
Volume 24, Issue 3, Pages 143-152Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/08958378.2011.649189
Keywords
Allethrin; epididymidis; oxidative stress; sperm maturation
Categories
Funding
- University Grants Commission, Government of India
- University of Hyderabad
- Council of Scientific and Industrial Research
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Objectives: Continuous inhalation of allethrin-based mosquito coil smoke may affect fertility, an aspect that has not received much attention. In this study, we attempt to understand the harmful effects on the male reproductive system caused by continuous exposure to allethrin-based mosquito coil smoke. Methods: Adult Wistar rats were allowed to inhale mosquito coil smoke for 15-180 days, and male reproductive tract tissues (caput, cauda, and testes) were collected. Using standard biochemical techniques, changes in oxidative stress (lipid peroxidation) and antioxidant status was measured. Histopathological analyses were carried out to assess pathomorphological damage in the caput, cauda, and testis. Real-time polymerase chain reaction was carried out to determine the expression pattern of the stress-response gene, p53, and the spermatogenic factors c-Kit, Scf, and Tgf-beta 1. Results: In rats exposed to allethrin-based mosquito coil smoke for 15-180 days, compared to the unexposed controls, lipid peroxidation was increased in the cauda and testes. The activity of antioxidant enzymes remained largely unchanged in the all the tissues analyzed. Histopathological analyses revealed loss of tubule architecture, epithelial cell disruption, increase in lumen size, interstitial edema, and presence of dead spermatozoa. p53 gene expression was differentially altered in the epididymis and testes. The expression of spermatogenic factors, namely, stem cell factor and its ligand c-Kit was unaltered though decreased levels of Tgf-beta 1 were observed. Conclusion: Results of this study demonstrate that prolonged exposure to allethrin-based mosquito coil smoke could lead to oxidative stress and compromise germ cell production.
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