ToxSci Advance Access originally published online on September 22, 2007
Toxicological Sciences 2007 100(2):504-512; doi:10.1093/toxsci/kfm245
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Reversibility of the Adverse Effects of 1-Bromopropane Exposure in Rats
* Department of Occupational and Environmental Health 466-8550
Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, 466-0065 Japan
School of Public Health, Anhui Medical University, Hefei, 230032 China
Department of Molecular Neurobiology, Institute for Developmental Research, Aichi Human Service Center, Kasugai, 480-0392 Japan
¶ Shanghai Institute of Planned Parenthood Research, Shanghai, 200032 China
|| Emeritus Professor, Nagoya University School of Medicine, Nagoya, Japan
||| Center for Reproductive Medicine, Toyohashi Municipal Hospital, Toyohashi, 441-8570 Japan
|||| Department of Human Functional Genomics, Life Science Research Center, Mie University, Tsu, 514-8507 Japan
1 To whom correspondence should be addressed at Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan. Fax: +81-52-744-2124. E-mail: gak{at}med.nagoya-u.ac.jp.
Received June 24, 2007; accepted September 17, 2007
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Abstract |
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Previous experiments indicated that 1-bromopropane (1-BP), an alternative to chloroflurocarbons, is neurotoxic and inhibits spermiation in the testis. Here we investigated the reversibility of the toxic effects of 1-BP in rats. Male Wistar rats were divided into three equal groups of 24 each and exposed by inhalation to 0, 400 or 1000 ppm of 1-BP for 6 weeks (8 hrs/day, 7 days/week). Eight rats from each group were sacrificed at the end of 6 weeks exposure, and at 4 and 14 weeks after the end of exposure, to assess the recovery processes. We studied sperm count, motility, morphology and testicular histopathology, as well as blood pressure, skin temperature and hindlimb muscle strength. At the end of 6 weeks of exposure to 1000 ppm (0 week recovery), testicular weight, epididymal weight, sperm count and motility were low, morphologically abnormal sperm were increased and spermatogenic cells showed diffuse degeneration. These changes did not show full recovery at 14 weeks recovery, with the exception of the prostate and seminal vesicular weights, which recovered back to control values. At 400 ppm, increased retained spermatids at 0 week recovery returned to normal at 4 weeks recovery. Exposure to 1000 ppm produced sustained reduction of hindlimb muscle strength at 14 weeks recovery, whereas normalization of the skin temperature and blood pressure was noted after transient changes. Our study showed that the effect of 1-BP on spermatogenesis is dose-dependent; low exposure inhibited spermiation and hormone-dependent organ weight reduction and these changes were transient, while a higher dose of 1000 ppm 1-BP caused persistent depletion of spermatogenic cells.
Key Words: neurotoxicity; reproductive toxicity; 1-bromopropane; spermatogenic cells; spermiation; 
-enolase.
This paper was presented in part at the 46th Annual Society of Toxicology Meeting in Charlotte, NC, in March 2007.
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