ISSN: 1405-888X ISSN-e: 2395-8723
Testosterone treatment positively regulates protein and mRNA levels of Mn-dependent superoxide dismutase enzyme in pancreatic islets of male rats (Rattus norvegicus)
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Keywords

androgens
antioxidant enzymes
oxidative stress
pancreatic beta cells
Rattus norvegicus

How to Cite

Sosa-Larios, T. C., Morales-Miranda, A., Palomar-Morales, M., Rojas-Ochoa, A., Rodríguez-Peña, N., & Morimoto, S. (2023). Testosterone treatment positively regulates protein and mRNA levels of Mn-dependent superoxide dismutase enzyme in pancreatic islets of male rats (Rattus norvegicus). TIP Revista Especializada En Ciencias Químico-Biológicas, 26. https://doi.org/10.22201/fesz.23958723e.2023.618

Abstract

The androgenic hormone testosterone protects against pharmacological-induced damage to pancreatic islets in rodent models of diabetes. The increased production of reactive oxygen species damage the pancreatic islets through oxidative stress and apoptosis. The precise protective mechanism of testosterone has yet to be determined. The aim of this study was to evaluate the effect of post-gonadectomy testosterone substitution on the expression of two key antioxidant enzymes, Mn-dependent superoxide dismutase and catalase. The protein expression of the enzymes was examined by immunohistochemistry in male rats: intact, gonadectomized, and gonadectomized followed by testosterone substitution. mRNA expression was analyzed by reverse transcription-quantitative polymerase chain reaction on pancreatic islets cultured with testosterone, dihydrotestosterone (DHT) or the vehicle. Testosterone increased the protein level of MnSOD in pancreatic tissue and its mRNA expression in cultured pancreatic islets. DHT (a non-aromatizing androgen) had similar effects. For catalase, only the mRNA expression increased by testosterone treatment. Testosterone induced overexpression of MnSOD protein and mRNA in pancreatic islets through a mechanism unrelated to androgen aromatization, most likely involving androgen receptors, demonstrating the implications of testosterone in preventing damage to insulin-producing cells by oxidative stress.

https://doi.org/10.22201/fesz.23958723e.2023.618
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