Exposure in utero to 2,2',3,3',4,6'-hexachlorobiphenyl (PCB 132) impairs sperm function and alters testicular apoptosis-related gene expression in rat offspring

Journal Article · Tue May 15 04:00:00 EDT 2007 · Toxicology and Applied Pharmacology

DOI:https://doi.org/10.1016/j.taap.2007.01.027· OSTI ID:20976935

Hsu, P -C ^[1]; Pan, M -H ^[2]; Li, L -A ^[3]; Chen, C -J ^[1]; Tsai, S -S ^[4]; Guo, Y L ^[5]

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1. Department of Safety, Health and Environmental Engineering, National Kaohsiung First University of Science and Technology, Kaohsiung, Taiwan (China)
2. Department of Seafood Science, National Kaohsiung Marine University, Kaohsiung, Taiwan (China)
3. Division of Environmental Health and Occupational Medicine, National Health Research Institutes, Zhunan, Taiwan (China)
4. Department of Veterinary Medicine, National Pingtung University of Science and Technology, Pingtung, Taiwan (China)
5. No. 1, Section 1, Jen-Ai Road, Department of Environmental and Occupational Medicine, National Taiwan University College of Medicine, Taipei 100, Taiwan (China)

Toxicity of the polychlorinated biphenyls (PCBs) depends on their molecular structure. Mechanisms by prenatal exposure to a non-dioxin-like PCB, 2,2',3,4',5',6-hexachlorobiphenyl (PCB 132) that may act on reproductive pathways in male offspring are relatively unknown. The purpose was to determine whether epididymal sperm function and expression of apoptosis-related genes were induced or inhibited by prenatal exposure to PCB 132. Pregnant rats were treated with a single dose of PCB 132 at 1 or 10 mg/kg on gestational day 15. Male offspring were killed and the epididymal sperm counts, motility, velocity, reactive oxygen species (ROS) generation, sperm-oocyte penetration rate (SOPR), testicular histopathology, apoptosis-related gene expression and caspase activation were assessed on postnatal day 84. Prenatal exposure to PCB 132 with a single dose of 1 or 10 mg/kg decreased cauda epididymal weight, epididymal sperm count and motile epididymal sperm count in adult offspring. The spermatozoa of PCB 132-exposed offspring produced significantly higher levels of ROS than the controls; ROS induction and SOPR reduction were dose-related. In the low-dose PCB 132 group, p53 was significantly induced and caspase-3 was inhibited. In the high-dose group, activation of caspase-3 and -9 was significantly increased, while the expressions of Fas, Bax, bcl-2, and p53 genes were significantly decreased. Gene expression and caspase activation data may provide insight into the mechanisms by which exposure to low-dose or high-dose PCB 132 affects reproduction in male offspring in rats. Because the doses of PCB 132 administered to the dams were approximately 625-fold in low-dose group and 6250-fold higher in high-dose group than the concentration in human tissue levels, the concentrations are not biologically or environmentally relevant. Further studies using environmentally relevant doses are needed for hazard identification.

• OSTI ID: 20976935
• Journal Information: Toxicology and Applied Pharmacology, Journal Name: Toxicology and Applied Pharmacology Journal Issue: 1 Vol. 221; ISSN TXAPA9; ISSN 0041-008X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ANIMAL TISSUES
APOPTOSIS
DIOXIN
DOSES
GENES
HEALTH HAZARDS
MOLECULAR STRUCTURE
OOCYTES
POLYCHLORINATED BIPHENYLS
PRENATAL EXPOSURE
PROGENY
PYRAZOLINES
RATS
REPRODUCTION
SPERMATOZOA
TESTES
TOXICITY