Abstract

Infertility has become an increasingly important health problem due to genetic, familial, hormonal, and congenital abnormalities, environmental and chemical reasons. This study aimed to investigate the effects of Panax ginseng (Pnx) root extract on cisplatin (CP) induced testicular damage of rats. Four animal groups were applied with different protocols as Control, Pnx (200 mg / kg), CP (7 mg / kg), and CP + Pnx (200 mg / kg). At the end of the experiment, the body and testicular weights of the rats were measured. While free/total testosterone, total antioxidant capacity (TAC), and total oxidative species (TOS) levels were analyzed in blood samples, apoptotic cells were marked by TUNEL staining in testicular samples of rats. According to the results, free/total testosterone and TAC levels were decreased while TOS levels increased in injured rats' plasma. On the other hand, seminiferous tubule diameters widened, and the number of apoptotic cells increased in rats' testis. These variables were significantly improved with the consumption of Pnx. As a result, Pnx has a significant protective effect on testicular tissue; however, further studies are needed to elucidate its action mechanism.

Highlights

  • Cisplatin (CP) is an alkylating chemotherapeutic agent used alone or in combination with antineoplastic agents in mouth, head, neck, endometrium, lung, ovarian, and testicular cancers (Dasari et al, 2014)

  • The purpose of this study is to examine the effects of Panax ginseng (Pnx), which has been used as a chemotherapeutic drug for centuries, on possible damages on the testis, and to develop an alternative treatment method in male infertility, which is a significant health problem today

  • There is no change in the ratio of right and left testis weight to body weight in the Pnx-treated healthy rats

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Summary

Introduction

Cisplatin (CP) is an alkylating chemotherapeutic agent used alone or in combination with antineoplastic agents in mouth, head, neck, endometrium, lung, ovarian, and testicular cancers (Dasari et al, 2014). Kidney functions are commonly followed in cancer chemotherapy, depending on CP (Barabas et al, 2008). CP is known to induce DNA damage by binding to the N7 reagent center on purine residues and rising apoptotic cell death by blocking cell division in cancer cells. Cancer cells cause more oxidation than normal cells with increased metabolic activity, oncogenic activation, and corruption of mitochondrial functions. Recent studies showed that CP induced genotoxicity and reproductive toxicity accompanied by severe oxidative stress (Aksu et al, 2016; Sadeghi et al, 2018). CP-induced animals exhibited lower sperm count and motility as well as higher abnormal sperm; testicular injury adversely affects spermatogenesis, sperm quality, and oxidative

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