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Selenium attenuates bisphenol A incurred damage and apoptosis in mice testes by regulating mitogen‐activated protein kinase signalling
Author(s) -
Kaur Sarvnarinder,
Saluja Muskaan,
Aniqa Aniqa,
Sadwal Shilpa
Publication year - 2021
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.13975
Subject(s) - oxidative stress , kinase , p38 mitogen activated protein kinases , superoxide dismutase , mapk/erk pathway , protein kinase a , catalase , apoptosis , chemistry , antioxidant , endocrinology , andrology , medicine , pharmacology , biochemistry , biology
Abstract Being a vital micronutrient, along with a trace element, selenium (Se) protects the cells from oxidative stress (OS) in the form of selenoproteins. Bisphenol A (BPA) is a xeno‐oestrogenic compound that adversely affects the spermatogenesis process by inducing oxidative stress, which ultimately leads to male infertility. Therefore, it is hypothesised that Se could protect against BPA‐induced OS, and further germ cell death by modifying mitogen‐activated protein kinase (MAPK) signalling. Male Balb/c mice were divided into four groups: Group I (C) (0.2 ppm Se), Group II (Se) (0.5 ppm Se), Group III (BPA) (0.2 ppm Se, and BPA = 1 mg/kg orally) and Group IV (Se + BPA) (0.5 ppm Se, and BPA = 1 mg/kg bodyweight orally). Results indicated that BPA‐treated animals demonstrated a marked decrease in antioxidant enzyme activities (superoxide dismutase, catalase, redox ratio), a marked elevation in the expressions of stress‐activated kinases (c‐Jun NH2‐terminal kinase (JNK), extracellular signal‐regulated kinase (ERK) and p38) and the expressions of pro‐apoptotic markers (caspase‐9, caspase‐8 and caspase‐3). However, Se supplementation considerably restored the antioxidant enzyme activities and lowered the expressions of stress‐activated kinases, which further down‐regulated the apoptosis. Thus, Se supplementation demonstrated to be effective against BPA provoked testicular damage.