The Efficiency of Chitosan Against Tert Butylhydroquinone (TBHQ)-Induced Neurobehavioral Changes and Toxicity Effects in Male Rats.

IF 3.1 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Frontiers in bioscience (Landmark edition) Pub Date : 2025-01-06 DOI:10.31083/FBL26871
Shahad Alahmadi, Mohammed Mufadhe Alanazi, Fawaz Alasmari, Wedad Saeed Al-Qahtani, Gadah Albasher
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Abstract

Background: We investigated chitosan's protective effects against tertiary butylhydroquinone (TBHQ)-induced toxicity in adult male rats, focusing on cognitive functions and oxidative stress in the brain, liver, and kidneys.

Methods: Rats were divided into four groups (n = 8/group): (1) Control, (2) Chitosan only, (3) TBHQ only, and (4) Chitosan + TBHQ.

Results: TBHQ exposure led to significant cognitive impairments and increased oxidative stress, marked by elevated malondialdehyde (MDA) and decreased superoxide dismutase (SOD) and glutathione (GSH) levels. Behavioral tests, including the Morris Water Maze (MWM) as well as Passive Avoidance Learning (PAL) tasks, confirmed memory and learning deficits in the TBHQ group. Histopathological analysis showed damage in the brain, liver, and kidney tissues of TBHQ-exposed rats. Chitosan treatment significantly mitigated these effects, reducing oxidative stress markers and preserving tissue integrity. These findings suggest that chitosan's antioxidant properties may provide a therapeutic benefit against TBHQ-induced neurotoxicity and organ damage.

Conclusions: These findings suggest that chitosan exerts potent neuroprotective effects, potentially through its antioxidant and anti-inflammatory properties, and could serve as a therapeutic agent against TBHQ-induced toxicity.

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壳聚糖对叔丁基对苯二酚(TBHQ)诱导的雄性大鼠神经行为改变的影响及其毒性作用。
背景:我们研究了壳聚糖对叔丁基对苯二酚(TBHQ)引起的成年雄性大鼠毒性的保护作用,重点研究了脑、肝和肾的认知功能和氧化应激。方法:将大鼠分为4组(n = 8/组):(1)对照组,(2)单壳聚糖组,(3)单壳六酚组,(4)壳聚糖+三酚组。结果:TBHQ暴露导致显著的认知障碍和氧化应激增加,其特征是丙二醛(MDA)升高,超氧化物歧化酶(SOD)和谷胱甘肽(GSH)水平降低。行为测试,包括莫里斯水迷宫(MWM)和被动回避学习(PAL)任务,证实了TBHQ组的记忆和学习缺陷。组织病理学分析显示,暴露于tbhq的大鼠脑、肝、肾组织均有损伤。壳聚糖处理显著减轻了这些影响,降低了氧化应激标志物并保持了组织完整性。这些发现表明,壳聚糖的抗氧化特性可能对tbhq诱导的神经毒性和器官损伤有治疗作用。结论:这些发现表明壳聚糖具有强大的神经保护作用,可能通过其抗氧化和抗炎特性,并可作为tbhq诱导毒性的治疗剂。
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