须达喹通过调节Nrf-2/Keap-1、炎症、类固醇生成和组织学特征减轻白化大鼠的百草枯睾丸毒性

IF 4.4 3区 医学 Q2 ENVIRONMENTAL SCIENCES Environmental Toxicology Pub Date : 2024-08-23 DOI:10.1002/tox.24408
Muhammad Umar Ijaz, Sana Imtiaz, Muhammad Faisal Hayat, Moazama Batool, Khalid A Al-Ghanim, Mian Nadeem Riaz
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引用次数: 0

摘要

百草枯(PQ)是一种有毒除草剂,会对包括男性生殖系统在内的重要器官产生不利影响。苏达其丁(SCN)是一种天然黄酮类化合物,具有广泛的生物潜力。本研究旨在调查 SCN 在避免 PQ 诱导的大鼠睾丸毒性方面的缓解潜力。研究人员将 48 只雄性大鼠(Rattus norvegicus)分成四组,包括对照组、PQ(5 毫克/千克)组、PQ + SCN(5 毫克/千克 + 30 毫克/千克)组和仅 SCN(30 毫克/千克)处理组。我们的研究结果表明,PQ 处理会降低核因子红细胞 2 相关因子 2(Nrf-2)及其抗氧化基因的表达,以及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽还原酶(GSR)和谷胱甘肽过氧化物酶(GPx)的活性,同时升高活性氧(ROS)和丙二醛(MDA)的水平。此外,PQ中毒会上调Keap-1的表达,同时下调3-β羟类固醇脱氢酶(3β-HSD)、17-β羟类固醇脱氢酶(17β-HSD)和类固醇生成急性调节蛋白(StAR)的表达。此外,接触 PQ 后精子畸形率增加。此外,接触 PQ 会降低血浆中睾酮、黄体生成素(LH)和促卵泡激素(FSH)的水平,同时增加白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、核因子卡巴 B(NF-κB)、白细胞介素-1β(IL-1β)和环氧化酶-2(COX-2)的水平。此外,PQ 处理会增加半胱氨酰天冬氨酸特异性蛋白酶-3(Caspase-3)和 Bcl-2 相关 X 蛋白(Bax)的表达,同时下调 B 细胞淋巴瘤-2(Bcl-2)的表达。此外,PQ 暴露破坏了睾丸组织的正常结构。然而,由于 SCN 具有抗氧化、抗炎和雄激素潜能,它能通过调节上述破坏作用显著保护睾丸组织。
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Sudachitin Alleviates Paraquat Instigated Testicular Toxicity in Albino Rats via Regulating Nrf-2/Keap-1, Inflammatory, Steroidogenic, and Histological Profile.

Paraquat (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.

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来源期刊
Environmental Toxicology
Environmental Toxicology 环境科学-毒理学
CiteScore
7.10
自引率
8.90%
发文量
261
审稿时长
4.5 months
期刊介绍: The journal publishes in the areas of toxicity and toxicology of environmental pollutants in air, dust, sediment, soil and water, and natural toxins in the environment.Of particular interest are: Toxic or biologically disruptive impacts of anthropogenic chemicals such as pharmaceuticals, industrial organics, agricultural chemicals, and by-products such as chlorinated compounds from water disinfection and waste incineration; Natural toxins and their impacts; Biotransformation and metabolism of toxigenic compounds, food chains for toxin accumulation or biodegradation; Assays of toxicity, endocrine disruption, mutagenicity, carcinogenicity, ecosystem impact and health hazard; Environmental and public health risk assessment, environmental guidelines, environmental policy for toxicants.
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