Selenium and Lycopene Attenuate Cisplatin-induced Testicular Toxicity Associated With Oxidative Stress in Wistar Rats

Salem, Emad A.; Salem, Neveen A.; Maarouf, Aref; Şerefoğlu, Ege Can; Hellstrom, Wayne J.G.

doi:10.1016/j.urology.2011.12.006

Cited by 69 publications

(49 citation statements)

References 24 publications

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“…Similar conclusions were drawn by Tamiselvan et al [18], Türk et al [49] and Salem et al [51] reporting that LYC administration resulted in a normalization of the antioxidant status together with a stabilization of SOD, CAT, GPx and GSH followed by a decrease of H 2 O 2 production and MDA synthesis in male reproductive cells and tissues.…”

Section: Discussionsupporting

confidence: 88%

Antioxidant efficiency of lycopene on oxidative stress - induced damage in bovine spermatozoa

Tvrdá

Kováčik

Paál

et al. 2016

J Animal Sci Biotechnol

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BackgroundLycopene (LYC) is a natural carotenoid with powerful reactive oxygen species (ROS) scavenging activities. The aim of this study was to investigate if lycopene has the ability to reverse ROS-mediated alterations to the motility, viability and intracellular antioxidant profile of bovine spermatozoa subjected to ferrous ascorbate (FeAA). Spermatozoa were washed out of fresh bovine semen, suspended in 2.9 % sodium citrate and subjected to LYC treatment (0.25, 0.5, 1 or 2 mmol/L) in the presence or absence of FeAA (150 μmol/L FeSO4 and 750 μmol/L ascorbic acid) during a 6 h in vitro culture. Spermatozoa motion characteristics were assessed using the SpermVision™ computer-aided sperm analysis (CASA) system. Cell viability was examined with the metabolic activity (MTT) assay, ROS generation was quantified via luminometry and the nitroblue-tetrazolium (NBT) test was applied to quantify the intracellular superoxide formation. Cell lysates were prepared at the end of the in vitro culture to investigate the intracellular activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) as well as the concentrations of glutathione (GSH) and malondialdehyde (MDA).ResultsFeAA treatment led to a reduced spermatozoa motility (P < 0.001), viability (P < 0.001) and a decline of the antioxidant capacity of spermatozoa (P < 0.001) but increased the ROS generation (P < 0.001), superoxide production (P < 0.001) and lipid peroxidation (P < 0.001). LYC administration resulted in a preservation of the spermatozoa motion parameters (P < 0.001), mitochondrial activity (P < 0.001) and antioxidant characteristics (P < 0.001 with respect to SOD; P < 0.01 in relation to CAT; P < 0.05 as for GPx and GSH) with a concentration range of 1 and 2 mmol/L LYC revealed to be the most effective.ConclusionsOur results suggest that LYC exhibits significant ROS-scavenging and antioxidant properties which may prevent spermatozoa alterations caused by oxidative stress, and preserve the functionality of male reproductive cells.

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Section: Discussionsupporting

confidence: 88%

Antioxidant efficiency of lycopene on oxidative stress - induced damage in bovine spermatozoa

Tvrdá

Kováčik

Paál

et al. 2016

J Animal Sci Biotechnol

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“…Although BPA did not change the body weights and relative organ weights, it exerted various subtle influences on the body. In the present study, we found oxidative stress was induced by the exposure in terms of the significant reduction of SOD and GSH‐Px, and the abnormal accumulation of MDA in both serum and testicular tissues (Salem et al, ). Oxidative stress as a mediator in apoptosis and autophagy has been well identified, and the important role of mitochondria in the processes is also widely accepted (Slater et al, ; Lee et al, ).…”

Section: Discussionsupporting

confidence: 55%

Bisphenol a induces autophagy and apoptosis concurrently involving the Akt/mTOR pathway in testes of pubertal SD rats

Quan

Wang

Duan

et al. 2016

Environmental Toxicology

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Bisphenol A (BPA), a typical endocrine disrupting chemical (EDC), has been proven to cause male reproductive toxicity. However, the precise mechanisms of this effect are still unclear. Puberty is a crucial period of reproductive development, and adolescents are more susceptible to xenobiotics. This research was designed to explore the mechanism of BPA toxicity on pubertal male reproduction. Rats were exposed to 0, 2, 10, 50 mg kg bw BPA, then the levels of sex hormones, oxidative stress, and semen quality were detected. HE staining, TUNEL assay and transmission electron microscopy were used to investigate the morphological changes, apoptosis, and autophagy in testes, respectively. Expressions of relevant genes and proteins were measured by RT-PCR, western blotting, and immunohistochemical staining. The results indicated that BPA exposure led to oxidative stress and endocrine disorders in pubertal male SD rats, caused apoptosis and autophagy in testes, and then damaged spermatogenesis ultimately. The Akt pathway was activated and the mTOR pathway was inhibited in the process. Taken together, BPA induced apoptosis and autophagy concurrently in pubertal testes, and this added a new layer to our understanding on male reproductive toxicity of BPA. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1977-1989, 2017.

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“…In the present study, a significant decrease in body and reproductive organs weights accompanied by marked histopathological alterations in the testicular tissue was observed in cisplatin treated rats, findings that are in agreement with previous work (Azu et al, 2010;Salem et al, 2012;Adejuwon et al, 2015). The reduction in reproductive organs weight is due to marked parenchymal atrophy in germinal cell layers, loss of maturation in the germinal cells and arrested spermatocytes at different stages of division which lead to tubular shrinkage in testicular tissues (Ilbey et al, 2009a; Beytur et al, 2012).…”

Section: Discussionsupporting

confidence: 94%

Protective Effect of L-Carnitine Against Cisplatin-Induced Testicular Toxicity in Rats

Eid

2016

Al-Azhar Journal of Pharmaceutical Sciences

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Testicular damage is one of the most deleterious effects whenever cisplatin (CIS) is employed in cancer chemotherapy. Oxidative stress has been proven to be involved in CIS induced toxicity. Thus, the current study explored the possible protective effect of L-carnitine (L-CAR) against cisplatin-induced testicular damage in rats. L-carnitine (500 mg/kg/day; i.p.) was injected for 15 days, whereas cisplatin (10 mg/kg; i.p.) was injected as a single dose at the 12 th day to induce testicular damage in adult male Sprague-Dawley rats. In the current study, CIS reduced the reproductive organs weight, sperm count, sperm motility and serum testosterone level beside a marked increase in the incidence of sperm abnormalities. In addition, it significantly increased malondialdehyde (MDA) and nitric oxide (NO) along with a marked decrease in testis reduced glutathione (GSH) content and superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities. At the same time, CIS administration resulted in marked elevation in tumor necrosis factor-α (TNF-α) production and nuclear factorkabba B (NF-κB) expression. These results were confirmed by histopathological examination. Treatment with L-CAR markedly attenuated cisplatin-induced injury by suppression of oxidative/nitrosative stress and inflammation, amendment of antioxidant defenses, as well as improvement of steroidogenesis, spermatogenesis and testicular histological features. This study suggests a novel therapeutic application for L-carnitine as a protective agent against cisplatininduced testicular toxicity through its promising anti-inflammatory and antioxidant capacities.

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Selenium and Lycopene Attenuate Cisplatin-induced Testicular Toxicity Associated With Oxidative Stress in Wistar Rats

Cited by 69 publications

References 24 publications

Antioxidant efficiency of lycopene on oxidative stress - induced damage in bovine spermatozoa

Antioxidant efficiency of lycopene on oxidative stress - induced damage in bovine spermatozoa

Bisphenol a induces autophagy and apoptosis concurrently involving the Akt/mTOR pathway in testes of pubertal SD rats

Protective Effect of L-Carnitine Against Cisplatin-Induced Testicular Toxicity in Rats

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