Reproductive parameters and oxidative stress status of male rats fed with low and high salt diet

Abstract

BACKGROUND:Deficiency of minerals and micronutrients has been reported to impair the process of spermatogenesis. Historically, salt has been used by women on their husbands to increase their libido, however, the role of salt diet on sperm parameters are yet to be ascertained.AIM:The present study was designed to determine the effect of low and high salt diet on sperm parameters, oxidative status and reproductive hormone levels of male rats.MATERIALS AND METHODS:A total of 18 rats were divided into three groups: Group I: (control) received 0.3% salt diet, Group II: low salt (received 0.14% salt diet) and Group III: high salt (received 8% salt diet). All animals were treated for 6 weeks; after which epididymal sperm parameters; oxidative stress markers (malondialdehyde, glutathione, catalase and superoxide dismutase) in the testes and epididymal tissues, as well as follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone levels were determined.RESULTS:The results showed decreased sperm count in the low salt diet rats while increased sperm count was observed in the high salt diet treated rats. Both low salt and high salt diet fed rats exhibited increased abnormal sperm cells and increased epididymal oxidative stress when compared with their respective control. FSH and testosterone levels were increased in the high salt fed rats while LH level was decreased when compared with the control values.CONCLUSION:This study suggests that both low and high salt diet play a negative role in the fertility of male rats.

High Salt Diet Affects the Reproductive Health in Animals: An Overview

“…Similar to previous studies, Iranloye et al [37] indicated that rats that received NaCl at 8% exhibited a relatively high MDA level in the epididymis compared to the controls. The activities of SOD, GSH, and CAT enzymes in testicular and epididymal tissues were significantly reduced by increased dietary salt in rats [37]. The high levels of MDA and SOD in the testis of rats fed a high salt diet can be attributed to free radical harm, confirming the harmful influences of the high salt intake on the reproductive patterns.…”

“…GSH and catalase activities did not significantly differ between the high salt and control groups [24]. Similar to previous studies, Iranloye et al [37] indicated that rats that received NaCl at 8% exhibited a relatively high MDA level in the epididymis compared to the controls. The activities of SOD, GSH, and CAT enzymes in testicular and epididymal tissues were significantly reduced by increased dietary salt in rats [37].…”

“…In addition, a significantly high percentage of abnormalities (p < 0.05) was detected in treated rats (8 per cent high salt diet) relative to control rats. Another study observed that rats fed the diet with high salt (8%) had a significant increase (p < 0.05) in sperm abnormalities, while no significant effects were detected in sperm motility with high or low salt diet [37].…”

“…Moreover, high levels of cortisol can reduce fertility [48], thus high sodium intake affects the reproductive function. Iranloye et al [37] documented a significant improvement in FSH and testosterone levels when rat were fed with a high salt diet, however, a remarkable decrease in LH was observed when compared with controls (p < 0.05). This issue still needs to be investigated.…”

Cyperus esculentusL. (tigernut) mitigates high salt diet‐associated testicular toxicity in Wistar rats by targeting testicular steroidogenesis, oxidative stress and inflammation

“…Fang, Zhong, Sun, and Zhou (2018) reported similar effects including decreased reproductive performance and mRNA expression of heat shock protein 70, the receptor tyrosine kinase and cyclin A which are key genes for spermatogenesis. HSD has also been reported to decrease luteinising hormone (LH) level and increase epididymal oxidative stress and abnormal sperm cells (Iranloye, Oludare, Morakinyo, Esume, & Ekeh, 2013). One mechanism by which HSD induces hypertension is by generation of reactive oxygen species which when generated in excess of the endogenous antioxidants causes oxidative stress (Dobrian, Schriver, Lynch, & Prewitt, 2003).…”