ToxSci Advance Access originally published online on January 30, 2008
Toxicological Sciences 2008 103(1):137-148; doi:10.1093/toxsci/kfn020
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Motorcycle Exhaust Induces Reproductive Toxicity and Testicular Interleukin-6 in Male Rats
* Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan, ROC
Institute of Veterinary Pathobiology, National Chung-Hsing University, Taichung, Taiwan, ROC
Taiwan Agricultural Chemicals and Toxic Substances Research Institute, Taichung, Taiwan, ROC
Department of Anesthesiology
¶ Department of Obstetrics and Gynecology, College of Medicine, National Taiwan University, Taipei, Taiwan, ROC
1 To whom correspondence should be addressed at Institute of Toxicology, College of Medicine, National Taiwan University, 1 Jen Ai Road, Section 1, Taipei, Taiwan, ROC. Fax: +886-2-2314-0217. E-mail: thueng{at}ntu.edu.tw.
Received December 13, 2007; accepted January 15, 2008
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Abstract |
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Motorcycle exhaust (ME) from two-stroke engines contains many toxicants and poses a potential health hazard. The major objectives of the present study were to investigate the male reproductive toxicity of ME and the underlying mechanisms of toxicity. Male Wistar rats were exposed to ME by inhalation 1 h each in the morning and afternoon, Monday through Friday. Exposures to 1:50 diluted ME for 4 weeks or to 1:10 diluted ME for 2 and 4 weeks showed concentration- and time-dependent decreases of testicular weight, spermatid number, and cauda epididymal sperm number. Subsequent studies were done using 4-week exposure to 1:10 diluted ME. ME caused histopathological changes including testicular spermatocytic necrosis and seminiferous tubule atrophy and cauda epididymal formation of clusters of pyknotic and necrotic sperm cells. ME-exposed male rats mated with untreated females showed decreases of male mating index and female fertility index and an increase of implantation site loss. ME decreased 7-ethoxycoumarin O-deethylase and superoxide dismutase activities but induced proinflammatory cytokine interleukin-6 (IL-6) messenger RNA (mRNA) in the testis. Male rats were exposed to ME with or without cotreatment with 50 mg/kg vitamin E orally for 4 weeks. ME decreased serum testosterone concentration. This effect was reversed by cotreatment with vitamin E. ME decreased testicular spermatid number and induced IL-6 mRNA and protein. These effects were also reversed by the vitamin E cotreatment. The present findings show that ME causes male reproductive effects and induces testicular IL-6 in rats by mechanisms involving induction of oxidative stress and inhibition of steroidogenesis.
Key Words: motorcycle exhaust; IL-6; testis; sperm; testosterone; oxidative stress; air pollution.