Lack of effect of butylparaben and methylparaben on the reproductive system in male rats

Abstract

Exposure to methyl- or butylparaben in the diet for eight weeks did not affect any male reproductive organs or parameters at exposures as high as 10,000 ppm, corresponding to a mean daily dose of 1,141.1+/-58.9 or 1,087.6+/-67.8 mg/kg/day for methyl- and butylparaben, respectively. The rapid metabolism of parabens by esterases probably explains why these weakly estrogenic substances elicit no in vivo effects when administered by relevant exposure routes (i.e., topical and oral).

Parabens in urine, serum and seminal plasma from healthy Danish men determined by liquid chromatography–tandem mass spectrometry (LC–MS/MS)

“…Some parabens have been shown to have weak estrogenic effects in vitro and in animal studies (Okubo et al, 2001;Byford et al, 2002;Darbre et al, 2002Darbre et al, , 2003Darbre et al, , 2004Lemini et al, 2003;Pugazhendhi et al, 2005). Furthermore, studies have shown effects on the male reproductive system, resulting in the reduction of testosterone levels and mature sperm counts, in rats and mice after in utero exposure to some parabens (Oishi, 2001(Oishi, , 2002(Oishi, , 2004Kang et al, 2002), whereas other studies could not confirm these effects (Hoberman et al, 2008;Taxvig et al, 2008). Recently it has been discussed whether parabens could have an adverse effect on the testis mitochondria function, followed by a decreased reproductive potential (Tavares et al, 2009).…”

Effect of Ginkgo biloba extract on sperm quality, serum testosterone concentration and histometric analysis of testes from adult Wistar rats

“…Oh and Chung (2004), reported the affinity of the main flavonoid constituents isolated from GBE (quercetin, kaempferol and isorhamnetin) with the human recombinant estrogenic receptors α (ER-α), particularly the β (ER-β) in vitro. Hence, an estrogenic overload would be expected to occur as a consequence of the binding of GBE constituents to the estrogenic receptors, resulting in alterations in the spermatogenic process as caused by other disruptors such as the parabens (Hoberman et al, 2008;Tavares et al, 2009), organoclorine pesticides (Bretveld et al, 2007;Uzun et al, 2009;Victor-Costa, et al, 2010), bisphenols (Sakaue et al, 2001) and phthalates (Hu et al, 2009;Saillenfait et al, 2009;Martino et al, 2010). However, the data observed in the testes of GBE treated-rats did not show any statistical difference in the mean gonadal weight, total and luminal diameters, and the height of the epithelium of the seminiferous tubules when compared to the control group and between the GBE treated groups.…”

“…Many substances including environmental contaminants have been related to the occurrence of adverse effects on the male reproductive system for acting as endocrine dysregulators, for instance, the parabens (Hoberman et al, 2008;Tavares et al, 2009), organoclorine pesticides (Bretveld et al, 2007;Uzun et al, 2009;Victor-Costa et al, 2010), bisphenols (Sakaue et al, 2001) and phthalates (Hu et al, 2009;Saillenfait et al, 2009;Martino-Andrade and Chaoud, 2010) can interfere with the male reproductive system by mimetizing the endogenous estrogenic action or changing its metabolism. The estrogenic effects of GBE and its main isolated flavonoid components (quercetin, kaempferol and isorhamnetin) were reported by Oh and Chung (2004).…”

Regulatory risk assessments

“…Thus the regulation seems unduly and unnecessarily restrictive of PP and BP use levels for children (and adults) !2 years. A further concern relates to the much relaxed requirements in young infants and neonates for MP and EP in that neither of these compounds has been evaluated in neonatal rats commencing with animals aged <PND 21 (Oishi 6 (PND 25 for MP and EP) and Hoberman et al 22 ( PND 22)). If the lack of earlystage male reproductive toxicity data (pre-PND 21) is not considered to impact on the SCCS assessment of MP and EP, why is a similar criterion not applied to PP and BP?…”