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Environmental toxicants on Leydig cell function
Published in C. Yan Cheng, Spermatogenesis, 2018
Leping Ye, Xiaoheng Li, Xiaomin Chen, Qingquan Lian, Ren-Shan Ge
Methoxychlor is another synthetic organochlorine pesticide used as an alternative to DDT. Methoxychlor has applications for protecting crops, ornamentals, livestock, and pets against fleas, mosquitoes, and cockroaches. Methoxychlor was banned in the European Union in 2002 and in the United States in 2003. However, it is still widely used in other countries (see reviews171,172). After being absorbed to mammalian bodies, methoxychlor can be metabolized into the toxic metabolite 2,2-bis(p-hydroxyphenyl)-1,1,1-trichloroethane (hydroxychlor).173 Methoxychlor may have multiple mechanisms to lower the testosterone biosynthesis by (1) blocking Leydig cell development, (2) downregulating Leydig cell steroidogenesis-related gene expressions, and (3) directly inhibiting the androgen-biosynthetic enzyme activities.
Pesticides induced oxidative stress and female infertility: a review
Published in Toxin Reviews, 2020
Jitender Kumar Bhardwaj, Meenu Mittal, Priyanka Saraf, Priya Kumari
The dose- and duration-dependent exposure to endosulfan and malathion determines its cellular and biochemical toxicity (Hiremath and Kaliwall 2002). Histological examination after endosulfan and malathion treatment in Wistar albino rat revealed that the size of ovarian tissue and number of healthy follicles was found to be declined but number of atretic follicles was increased. Biochemical analysis showed that MDA level was elevated and act as an indicator of free radicals generated during the metabolism and their lipid peroxidation inducing damage, after endosufan and malathion treatment (Koc et al.2009). Similarly mancozeb, carbfuran, and chlorodecon showed dose-dependent effect with increase in atretic follicles and decrease in number of healthy follicles (Rockett et al.2006, Koc et al.2009). Methoxychlor causes abnormality in folliculogenesis (Gupta et al.2009).
Methoxychlor metabolite HPTE alters viability and differentiation of embryonic thymocytes from C57BL/6 mice
Published in Journal of Immunotoxicology, 2018
Lucie Leung-Gurung, Priscilla Escalante Cobb, Faraj Mourad, Cristina Zambrano, Zachary Muscato, Victoria Sanchez, Kanya Godde, Christine Broussard
Methoxychlor has been shown to be metabolized in a variety of organisms and to enhance its own metabolism (Li et al. 1995; Stuchal et al. 2006). The primary metabolite of MXC is 1,1,1-trichloro-2,2-bis(4-hydroxyphenyl) ethane (HPTE). While HPTE has been shown to be more estrogenic than MXC (Bulger et al. 1978; Ousterhout et al. 1981; Shelby et al. 1996; Hodges et al. 2000), little work has been done to specifically elucidate effects of HPTE on exposed animals or to measure levels of HPTE generated in MXC-treated animals. Without an understanding of conversion efficiency in animals, discrepancies in results are difficult to reconcile, particularly when variations in dose can lead to differences in response. For example, in a uterine cell line, HPTE induced proliferation at nM doses and growth inhibition at μM doses (Hewitt and Korach 2011). Lastly, none of the few studies that probed effects of HPTE directly addressed the impact of HPTE on immune system development, even though HPTE is the likely mediator of MXC effects.
In vivo assessment of respiratory burst inhibition by xenobiotic exposure using larval zebrafish
Published in Journal of Immunotoxicology, 2020
Drake W. Phelps, Ashley A. Fletcher, Ivan Rodriguez-Nunez, Michele R. Balik-Meisner, Debra A. Tokarz, David M. Reif, Dori R. Germolec, Jeffrey A. Yoder
Previous studies have shown that methoxychlor is able to inhibit antibody production in rodent models (Chapin et al. 1997; Hayashi et al. 2013), indicating potential toxicity to the adaptive immune system. However, in the zebrafish RBA, methoxychlor inhibited the respiratory burst, indicating this agent also impacts innate immunity. To our knowledge, this study is the first to show that methoxychlor suppresses the respiratory burst. The current observations are supported by a previous study that showed that exposing a mouse macrophage cell line to methoxychlor reduced interferon (IFN)-β signaling after lipopolysaccharide challenge (Ohnishi et al. 2008).