Dioxin-Induced Changes in Epididymal Sperm Count and Spermatogenesis

Abstract

BackgroundA 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 sourcesWe performed a PubMed search using relevant search terms linking dioxin exposure with adverse effects on reproduction and spermatogenesis.Data synthesisDevelopmental 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.ConclusionsAnimal 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.

Ancestral TCDD exposure promotes epigenetic transgenerational inheritance of imprinted gene Igf2: Methylation status and DNMTs

“…Human and rodent research of dioxins has proven that exposures that exhibit any or no severe impact during development can cause serious influences at a later stage of life in the offspring (Ahmed, 2011;Foster et al, 2010;Schantz et al, 1996;Winneke et al, 2013). These findings are quite consistent with the Barker hypothesis (Barker, 1990).…”

Silver nanoparticles effects on epididymal sperm in rats

“…AgNPs action in the epididymis seems to be similar to that of other xenobiotics including dioxane (e.g. TCDD), which increase free radicals production and reduce antioxidant potential in the epididymis and epididymal sperm (Latchoumycandane et al, 2003;Foster et al, 2010). Induction of the oxidative stress is one of the most commonly proposed mechanisms of NPs toxicity.…”

Dioxin‐Activated AHR: Toxic Responses and the Induction of Oxidative Stress

“…Several reviews, including various chapters in this book, have summarized the adverse health effects associated with exposure to dioxins [92,97,[102][103][104][105][106][107]. In summary, those effects include, but are not limited to, chloracne, various cancers, thyroid dysfunction, reproductive and developmental defects, diabetes, compromised immune functions, impaired neurodevelopment, liver damage, and wasting syndrome.…”