Sudachitin Alleviates Paraquat Instigated Testicular Toxicity in Albino Rats via Regulating Nrf‐2/Keap‐1, Inflammatory, Steroidogenic, and Histological Profile

Author:

Ijaz Muhammad Umar1ORCID,Imtiaz Sana1,Hayat Muhammad Faisal1,Batool Moazama2,Al‐Ghanim Khalid A.3,Riaz Mian Nadeem4

Affiliation:

1. Department of Zoology, Wildlife and Fisheries University of Agriculture Faisalabad Pakistan

2. Department of Zoology Govt. College Women University Sialkot Pakistan

3. Department of Zoology, College of Science King Saud University Riyadh Saudi Arabia

4. Texas A & M University College Station Texas USA

Abstract

ABSTRACTParaquat (PQ) is a noxious herbicide which adversely affects the vital organs including male reproductive system. Sudachitin (SCN) is a naturally occurring flavonoid that demonstrates a wide range of biological potentials. The current study was designed to investigate the alleviative potential of SCN to avert PQ‐induced testicular toxicity in rats. Forty‐eight male rats (Rattus norvegicus) were apportioned into four groups including control, PQ (5 mg/kg), PQ + SCN (5 mg/kg + 30 mg/kg), and SCN (30 mg/kg) only treated group. Our findings elucidated that PQ treatment reduced the expression of nuclear factor erythroid 2‐related factor 2 (Nrf‐2) and its antioxidant genes as well as the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GSR) and glutathione peroxidase (GPx), while elevating the levels of reactive oxygen species (ROS), and malondialdehyde (MDA). Furthermore, PQ intoxication upregulated the expressions of Keap‐1 while downregulating the expression of 3‐beta hydroxysteroid dehydrogenase (3β‐HSD), 17‐beta hydroxysteroid dehydrogenase (17β‐HSD), and steroidogenic acute regulatory protein (StAR). Moreover, sperm anomalies were increased following the exposure to PQ. Besides, PQ exposure decreased the levels of plasma testosterone, luteinizing hormone (LH), and follicle stimulating hormone (FSH) while increasing the levels of interleukin‐6 (IL‐6), tumor necrosis factor‐alpha (TNF‐α), nuclear factor‐kappa B (NF‐κB), interleukin‐1beta (IL‐1β), and cyclooxygenase‐2 (COX‐2). Additionally, PQ treatment escalated the expressions of cysteinyl aspartate‐specific proteases‐3 (Caspase‐3) and Bcl‐2‐associated X‐protein (Bax) while downregulating the expressions of B‐cell lymphoma‐2 (Bcl‐2). Furthermore, PQ exposure disrupted the normal architecture of testicular tissues. However, SCN treatment remarkably protected the testicular tissues via regulating the aforementioned disruptions owing to its antioxidant, anti‐inflammatory, and androgenic potential.

Publisher

Wiley

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