Reproductive toxic impact of subchronic treatment with combined butylparaben and triclosan in weanling male rats

Abstract

The effect of treatment with combined butylparaben and triclosan on male gonadal toxicity in weanling rats was investigated. All treated groups experienced atrophy in the ventral prostate and seminal vesicle, likewise significant depletion in the number and motility of sperm. Given individually or combined butylparaben and triclosan, significantly decreased testosterone, luteinizing hormone, and follicle-stimulating hormone levels. Individual treatment with tested compounds caused significant elevation in the E level, whereas combined treatment did not alter the E level. Testicular DNA damage was recorded in all treated groups. Moreover, the testicular malondialdehyde level was significantly elevated, along with a significant decrease in catalase enzyme activity in all treated groups. Superoxide dismutase enzyme activity was significantly decreased in the butylparaben-treated group, increased in the triclosan-treated group, and nonsignificantly changed the butylparaben-triclosan-treated group. The combined treatment produced an endocrine disturbance with a concomitant induction of testicular oxidative stress, which may represent a common mechanism of endocrine disruptor-mediated dysfunction.

Butylparaben Is Toxic to Porcine Oocyte Maturation and Subsequent Embryonic Development Following In Vitro Fertilization

“…Γ-H2AX has been used as a biomarker for DNA damage caused by cytotoxic chemical agents [38]. Previous studies reported that BP induced DNA damage in rats and humans [9,39]. Consistent with previous studies, our results demonstrated that the proportion of γ-H2AX-positive oocytes was significantly higher in the BP-treated group than the control group, indicating that BP exposure may attenuate oocyte maturation by disrupting DNA integrity.…”

Triclosan: An Update on Biochemical and Molecular Mechanisms

“…In rat thymocytes, superoxide anions were found to be elevated following TCS treatment [102] which, as Yueh et al [103] showed, was met with increased expression of key antioxidant enzymes including HO-1, NQO-1, and glutathione S-transferase (GST) in mouse liver. Evidence for testicular DNA damage, elevated malondialdehyde (MDA), and superoxide dismutase (SOD), in addition to diminished catalase (CAT), was related to TCS treatment in weanling rats [104]. Similarly, in lung homogenates of female albino rats, TCS was found to induce lipid peroxidation and severely deplete the levels of other crucial antioxidants: SOD, CAT, and glutathione (GSH) [105].…”

“…With regard to the androgenic properties of TCS, it was revealed that TCS interferes with testosterone- (TSN-) related transcription but promotes that dependent on androgen [181, 182]. In a recent in vivo study on weanling male rats, Riad et al [104] reported that TCS, either alone or combined with butylparaben, reduced TSN, leutinizing hormone (LH), and follicle-stimulating hormone (FSH), while increased E2 was observed upon single TCS administration Also, TCS-induced proliferation and migration of LNCaP cells were significantly reduced in presence of bicalutamide, an androgen receptor (AR) antagonist [77]. These findings support a previous report by Ahn et al [183] in which 1 μ M TCS reduced E2-induced ER activation by 50% and AR in human BG1Luc4E2 ovarian adenocarcinoma cells and T47D-ARE breast cancer cells, respectively.…”

Histological, immunohistochemical and biochemical study of the effect of triclosan and its withdrawal on cauda epididymis of adult albino rat

“…These hormones are essential for the process of spermatogenesis, which finally resulted in inhibition of spermatogenesis and decreased number of sperms with bad quality of semen [10] . Additionally, Riad et al [34] reported that TCS has significantly decreased the number and motility of sperm in weanling male rats as well as significantly decreased the testosterone level. They attributed this finding to the induction of testicular oxidative stress by TCS.…”