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Physiological Adaptation to Simultaneous Chronic Exposure to High-Fat Diet and Dichlorodipheniletylhene (DDE) in Wistar Rat Testis

1
Department of Biology, University of Naples, Federico II, 80126 Naples, Italy
2
Department of Chemistry and Biology “Adolfo Zambelli”, University of Salerno, 84084 Fisciano, Italy
3
Department of Science and Technologies, University of Naples, Parthenope, 80133 Naples, Italy
*
Author to whom correspondence should be addressed.
Cells 2019, 8(5), 443; https://doi.org/10.3390/cells8050443
Received: 18 March 2019 / Revised: 5 May 2019 / Accepted: 9 May 2019 / Published: 10 May 2019
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Stress Responses)
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Abstract

Environmental chemicals can be introduced by consuming contaminated foods. The environmental chemical dichlorodiphenyldichloroethylene (DDE), a persistent metabolite of dichlorodiphenyltrichloroethane (DDT), can affect spermatogenesis. Our study aims to evaluate, by using spectrophotometric analyses, western blot, and immunohistochemistry, the adaptive responses in testis of adult rats treated with a non-toxic dose of DDE, alone or in association with a high-fat diet (HFD). Four experimental groups were performed: N (normal diet); D (HFD); D + DDE (HFD + DDE); N + DDE (normal diet + DDE). D group showed a reduction in antioxidant capacity, and increases in lipid peroxidation, apoptosis, and proliferation associated with morphological impairment. A reduction in androgen receptor (AR) and serum testosterone levels were also found. DDE-treated groups exhibited higher lipid peroxidation levels compared to N and D, associated with pronounced defect in antioxidant capacity, apoptosis, cellular proliferation, as well as with tissue damage. Moreover, decreases in AR and serum testosterone levels were found in DDE-treated groups vs. N and D. In conclusion, HFD and DDE produced cellular stress leading to antioxidant impairment, apoptosis, and decreases in AR and serum testosterone levels associated with tissue damage. Cellular proliferation could be used as an adaptation to counterbalance the occurred damage, maintaining a pool of tubules that follow physiological maturation. View Full-Text
Keywords: environmental pollutants; hyperlipidic diet; oxidative stress; apoptosis; cell proliferation; androgen receptor environmental pollutants; hyperlipidic diet; oxidative stress; apoptosis; cell proliferation; androgen receptor
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Migliaccio, V.; Sica, R.; Scudiero, R.; Simoniello, P.; Putti, R.; Lionetti, L. Physiological Adaptation to Simultaneous Chronic Exposure to High-Fat Diet and Dichlorodipheniletylhene (DDE) in Wistar Rat Testis. Cells 2019, 8, 443.

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