Effect of syringic acid on oxidative stress, autophagy, apoptosis, inflammation pathways against testicular damage induced by lead acetate.

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Date

2023

Journal Title

Journal ISSN

Volume Title

Publisher

Elsevier GmbH

Access Rights

info:eu-repo/semantics/embargoedAccess

Abstract

Heavy metals are one of the environmental pollutants. Lead (Pb) is one of the most common of these heavy metals. In this study, it was aimed at investigating the effects of syringic acid (SA) against testicular toxicity in rats administered lead acetate (PbAc). Methods: In the present study, a total of 35 Sprague-Dawley rats, 7 in each group, were used. The rats were divided into 5 groups, with 7 male rats in each group. Rats were given PbAc and SA orally for 7 days. The effects of PbAc and SA on epididymal sperm quality and apoptosis, inflammation, oxidative stress and histopathological changes in testicular tissue were determined. Results: While PbAc disrupted the seminiferous tubules and produced atrophic images, SA corrected these histological abnormalities. PbAc adminisration significantly reduced the levels of SOD, GSH, GPx, CAT, NRF-2 and NQO1 and significantly increased the levels of MDA and 8-OHdG in the testicular tissue of rats, while SA improved this situation. NF-?B, TNF-?, IL-1?, NLRP3, RAGE, ATF6, PERK, IRE1, CHOP, and GRP78 genes expression levels increased with PbAc administration, however these levels decreased with SA administration. In addition, PbAc increased the levels of apoptotic markers Bax, Caspase-3 and APAF-1 and decreased the level of Bcl-2, while SA improved this situation. It was observed that PbAc significantly reduced sperm quality in rats, while SA positively affected sperm quality. Conclusion: As a result, SA administered against PbAc-induced testicular dysfunction in rats can provide effective protection at doses of 25 mg/kg/bw and 50 mg/kg/bw.

Description

Keywords

Apoptosis, Lead Acetate, Oxidative Stress, Syringic Acid, Testis, Rat

Journal or Series

Journal of Trace Elements in Medicine and Biology

WoS Q Value

Scopus Q Value

Q1

Volume

80

Issue

Citation