Effects of different DDE exposure paradigms on testicular steroid hormone secretion and hepatic oxidative stress in male Long-Evans rats

Molina, Erica M; Kavazis, Andreas N.; Mendonça, Mary T.; Akingbemi, Benson T.

doi:10.1016/j.ygcen.2021.113963

Cited by 4 publications

(6 citation statements)

References 51 publications

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Section: Methodsmentioning

confidence: 99%

“…Prepubertal Long–Evans male rats were given water containing environmentally relevant DDE doses (0, 0.1, and 10 µg/L of drinking water; [9]) from 21 to 49 days of age ( n = 12/group). These doses were found to decrease serum and testicular testosterone (T) in a previous study [9]. Animals were maintained under constant conditions of light (12 L:12 D) and temperature (20–23.38°C) with free access to pelleted food (soy- and alfalfa-free diet, 2020X, Harlan-Teklad, Indianapolis, IN) and water.…”

Section: Methodsmentioning

confidence: 99%

“…In addition, Blanco-Munoz et al [7] documented effects of chronic DDT exposure in humans at the gonadal, pituitary, and hypothalamic levels, indicating that the mechanisms by which DDT causes its effects are still unclear and require further study. To explore the potential mechanisms of action seen in our previous field and lab studies [8], we exposed male rats to environmentally relevant DDE doses extrapolated from our field study [9]. We found that DDE exposure of prepubertal (21–35 days of age) and pubertal rats (35–49 days of age) caused animals at both age groups to exhibit decreased serum T and testicular T production in a nonmonotonic dose–response that has been reported for many endocrine disruptors [9, 10].…”

Section: Introductionmentioning

confidence: 99%

“…To explore the potential mechanisms of action seen in our previous field and lab studies [8], we exposed male rats to environmentally relevant DDE doses extrapolated from our field study [9]. We found that DDE exposure of prepubertal (21–35 days of age) and pubertal rats (35–49 days of age) caused animals at both age groups to exhibit decreased serum T and testicular T production in a nonmonotonic dose–response that has been reported for many endocrine disruptors [9, 10]. However, pituitary luteinizing hormone-beta and follicle stimulating hormone-beta protein expression, i.e.…”

Section: Introductionmentioning

confidence: 99%

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Effects of chronic dichlorodiphenyldichloroethylene exposure on testosterone secretion and steroidogenic pathway in the male gonad

Molina

Kavazis

Mendonça

et al. 2023

Biology of Reproduction

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Endocrine disrupting chemicals (EDCs) are still found in the environment and/or in consumer products. These agents have the capacity to mimic and/or antagonize endogenous hormones and thus perturb the endocrine axis. The male reproductive tract expresses steroid hormone (androgen and estrogen) receptors at high levels and is a major target for EDCs. In the present study, Long-Evans male rats were exposed to dichlorodiphenyldichloroethylene (DDE), a metabolite of dichlorodiphenyltrichloroethane (DDT) and a chemical present in the environment, in drinking water at 0.1 and 10 μg/L for four weeks. At the end of exposure, we measured steroid hormone secretion and analyzed steroidogenic proteins, including 17β-hydroxysteroid dehydrogenase (17 β-HSD), 3β-hydroxysteroid dehydrogenase (3β-HSD), steroidogenic acute regulatory protein (StAR), aromatase and the LH receptor (LHR). We also analyzed Leydig cell apoptosis ((poly-(ADP-ribose) polymerase (PARP) and caspase-3 in the testes. Testicular testosterone (T) and 17β-estradiol (E2) were both affected by exposure to DDE by displaying altered steroidogenic enzyme expression. DDE exposure also increased expression of enzymes mediating the pathway for programmed cell death, including caspase 3, pro-caspase 3, PARP and cleaved PARP (cPARP). Altogether, the present results demonstrate that DDE directly and/or indirectly can target specific proteins involved in steroid hormone production in the male gonad and suggest that exposure to environmentally relevant DDE levels has implications for male reproductive development and function. Summary: Exposure to environmentally relevant DDE levels has implications for male reproductive development and activity due to its ability to disrupt T and E2 levels when exposed to DDE.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of chronic dichlorodiphenyldichloroethylene exposure on testosterone secretion and steroidogenic pathway in the male gonad

Molina

Kavazis

Mendonça

et al. 2023

Biology of Reproduction

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show abstract

“…As a large part of Endocrine Disruptor Chemicals (EDCs), pesticides can disturb endocrine homeostasis through various approaches. DDE (1,1-dichloro-2,2-bis( p -chlorophenyl) ethane) is an antagonist to the androgen receptor [ 48 ], and DDT (2Dichlorodiphenyltrichloroethane) can separate the thyrotropin receptor from lipid raft anchored in the cell membrane to inhibit downstream stimulation and internalization of thyroid hormone, causing thyroid dysfunction in rodents, birds, amphibians and fish [ 3 ]. Both can act as estrogen receptor agonists and promote estrogen receptor production.…”

Section: Mechanisms and Hazards Of Pesticidesmentioning

confidence: 99%