Selenium attenuates diclofenac‐induced testicular and epididymal toxicity in rats

Abstract

Diclofenac is a nonsteroidal anti-inflammatory drug (NSAID) derivative of phenylacetic acid, which elicits its therapeutic effects via inhibition of cyclooxygenase (Ortiz, 2017; Patrignani & Patrono, 2015). Diclofenac is globally used by millions of people mainly for the treatment of pain, inflammation, degenerative joint disease, rheumatoid arthritis, dysmenorrhoea and trauma (Ahmed et al., 2019; Aygun, Kaplan, Odaci, Onger, & Altunkaynak, 2012). Indeed, global diclofenac consumed yearly has been estimated to be approximately 940 tons (Zhang, Geissen, & Gal, 2008). Although diclofenac is an effective chemotherapeutic drug, its harmful effects in both animals and humans are associated with inhibition of prostaglandin biosynthesis. Specifically, diclofenac-mediated nephropathy, hepatotoxicity and ulceration, which are well-documented, have been related to the induction of oxidative damage (Ahmed, Gad, & El-Raouf, 2017;

Chlorogenic acid co‐administration abates tamoxifen‐mediated reproductive toxicities in male rats: An experimental approach

“…Microscopic assessment of the examined organs‐testis and epididymis‐sections was performed following Bancroft and Gamble’s methods and reported in the literature (Bancroft & Gamble, 2008; Owumi, Aliyu‐Banjo, et al, 2020). The testes and epididymis were carefully removed and fixed with Bouin’s solution.…”

N ‐acetyl cysteine co‐treatment abates perfluorooctanoic acid‐induced reproductive toxicity in male rats

“…A total of 400 spermatozoa from each rat were tallied and allotted to different classes of sperm morphological abnormalities. Sperm viability was determined by staining with nigrosin (10%) and eosin (0.7%) in a solution containing 0.9 g of sodium chloride according to the protocol of Mortimer and as previously reported (Mortimer, 1994; Owumi, et al., 2020). The suspension was incubated at room temperature for 30 min and subsequently transferred and smeared on a labelled microscopic slide with a coverslip in duplicates.…”

Selenium attenuates bisphenol A incurred damage and apoptosis in mice testes by regulating mitogen‐activated protein kinase signalling

“…Owumi et al. (2020) also reported the protective effect of Se (dose = 0.125 and 0.25 mg/kg) in terms of restoring sperm concentration and motility, hormonal levels (luteinising hormone and testosterone) in rats against toxicity induced by diclofenac. Our previous study showed the protective role of Se supplementation on BPA incurred testicular damage in terms of decreasing OS (revealed through decreased ROS and LPO levels and increased GSH‐Px activity) and apoptosis (revealed through histo‐architectural analysis of testes through haematoxylin and eosin (Hx & E) and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) analysis) (Kaur et al., 2018).…”