Academic journal article Environmental Health Perspectives

Dioxin-Induced Changes in Epididymal Sperm Count and Spermatogenesis

Academic journal article Environmental Health Perspectives

Dioxin-Induced Changes in Epididymal Sperm Count and Spermatogenesis

Article excerpt

BACKGROUND: A single in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on gestation day 15 decreased epididymal sperm count in adult rats and thus was used to establish a tolerable daily intake for TCDD. However, several laboratories have been unable to replicate these findings. Moreover, conflicting reports of TCDD effects on daily sperm production suggest that spermatogenesis may not be as sensitive to the adverse effects of TCDD as previously thought.

Data SOURCES: We performed a PubMed search using relevant search terms linking dioxin exposure with adverse effects on reproduction and spermatogenesis.

DATA SYNTHESIS: Developmental exposure to TCDD is consistently linked with decreased cauda epididymal sperm counts in animal studies, although at higher dose levels than those used in some earlier studies. However, the evidence linking in utero TCDD exposure and spermatogenesis is not convincing.

CONCLUSIONS: Animal studies provide clear evidence of an adverse effect of in utero TCDD exposure on epididymal sperm count but do not support the conclusion that spermatogenesis is adversely affected. The mechanisms underlying decreased epididymal sperm count are unknown; however, we postulate that epididymal function is the key target for the adverse effects of TCDD.

Key WORDS: development, dioxin, endocrine, reproduction, spermatogenesis. Environ Health Perspect 118:458-464 (2010). doi:10.1289/ehp.0901084 [Online 17 December 2009]

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Dioxins are lipophilic chemicals that resist biological and environmental degradation, making them persistent in the environment. Seventy-five dioxin congeners and 135 furan congeners comprise the complex mixture of dioxins, of which 7 and 10 congeners, respectively, are capable of binding to and activating the aryl hydrocarbon receptor (AhR) (Van den Berg et al. 2006). Of the 209 polychlorinated biphenyl (PCR) congeners, 12 have the potential to activate the AhR (Van den Berg et al. 2006). Among these, 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) is the most toxic environmental contaminant in animal studies (Denison and Nagy 2003) and thus is significant for human health (Birnbaum 1994; Larsen 2006; Schecter et al. 2006).

Dioxins are by-products of industrial processes such as chlorine bleaching of pulp and paper, the manufacture of certain pesticides, and incineration of medical waste and plastics (Anderson and Fisher 2002; Hewitt et al. 2006; Lin et al. 2006; Thornton et al. 1996). Resistance to degradation leads to bio-accumulation and biomagnification of dioxins in the food chain. Inclusion of animal fat in animal feed is another route of dioxin entry to the food supply and a source of exposure (Hoogenboom et al. 2007). Human exposure is primarily through consumption of contaminated food, especially high-fat foods such as milk, cheese, meat, some fish, fast foods, and breast milk (Schecter and Li 1997; Schecter et al. 1997, 1998a, 1998b, 2001). Residue levels have been measured in the serum of pregnant Canadian women with a mean [+ or -] SE of 0.34 [+ or -] 0.01 pg TCDD/g lipid (Foster et al. 2005), lower than the serum concentrations measured in pregnant German women (range, 4.34-97.3 pg TCDD/g lipid; Wittsiepe et al. 2007) and women from central Taiwan (mean, 6.7 pg TCDD/g lipid; Wang et al. 2004). The different concentrations in these studies reflect differences in measurement techniques; a gene reporter assay [chemical-activated luciferase gene expression (CALUX) assay] and high-resolution mass spectrometry have been used to quantify World Health Organization (WHO) toxic equivalence quotient concentrations or dioxin-like activity. Regardless, these studies demonstrate that the fetus is exposed to dioxin-like chemicals during a critical window of development. The half-life of dioxin ranges from 5.8 to 14.1 years in humans and is influenced by body composition, with higher body fat associated with a longer half-life (Michalek et al. …

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