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Protein carbonyl, 3β‐, and 17β‐hydroxysteroid dehydrogenases in testes and serum FSH, LH, and testosterone levels in zinc deficient Wistar rats
Author(s) -
Kumari Deepa,
Nair Neena,
Bedwal Ranveer Singh
Publication year - 2012
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.1020
Subject(s) - medicine , zinc , endocrinology , testosterone (patch) , hormone , hydroxysteroid dehydrogenase , dehydrogenase , zinc deficiency (plant disorder) , biology , secretion , chemistry , enzyme , biochemistry , organic chemistry
The present study evaluated protein oxidation, alteration in hydroxysteroid dehydrogenases (3β‐ and 17β HSD) in testes and serum hormonal profiles of dietary zinc deficient Wistar rats. Pre‐pubertal rats were divided into three groups: zinc control (ZC), pairfed (PF), and zinc deficient (ZD) and fed 100 ppm (ZC and PF groups) and 1.0 ppm (ZD group) zinc diet for 2‐ and 4‐weeks. The testes from zinc deficient groups exhibited significant increase in total protein (2 weeks) and protein carbonyl (2‐ and 4‐weeks) concentration as well as 3β‐ and 17β‐hydroxysteroid dehydrogenase activities (4 weeks), whereas a significant decrease was recorded in total protein (testes 4 weeks; serum 2‐ and 4‐weeks), total zinc (testes and serum 2‐ and 4‐weeks), 3β‐ and 17β‐hydroxysteroid dehydrogenase activities (testes 2 weeks), and serum hormonal profiles (FSH and testosterone 2‐ and 4‐weeks). However, LH was below the detectable limits. These results reflect that zinc deficiency during pre‐pubertal period affected total protein and zinc status, elevates protein oxidation, and causes dysregulation of the hydroxysteroid dehydrogenases. Low level of zinc attenuated the gonadal physiology which indicates that the metabolic regulation of testes is mediated by combined effects of a specific response (caused by decreased zinc concentration) and a nonspecific response (inhibition of gonadotrophin secretion). All these contribute to testicular dysfunction. © 2012 International Union of Biochemistry and Molecular Biology, Inc.