Emeninwa Chiedu Onyinye, Apiamu Augustine, Asagba Samuel Ogheneovo
Department of Biochemistry, Faculty of Science, Delta State University of Science and Technology, Ozoro, Nigeria.
Department of Biochemistry, Faculty of Science, Delta State University, Abraka, Nigeria.
Biol Trace Elem Res. 2025 Apr 23. doi: 10.1007/s12011-025-04622-0.
The study evaluated the biochemical and histopathological alterations of subacute nickel (Ni) and cadmium (Cd) exposure on the gastrointestinal and ocular systems of male Wistar albino rats via ingestion of contaminated water. Four groups of six rats each were exposed to uncontaminated water (group A as control), 100 mg/L of Cd (group B), 100 mg/L of Ni (group C), and a combination of 100 mg/L Cd and Ni (group D) for 28 days. The stomach, intestinal, and ocular weights were recorded and were significantly reduced (p ≤ 0.05) in the treatment groups when compared to the control, but the effect was profound in group D rats, as compared with groups B and C rats. The assessed amylase, lipase, and alkaline phosphatase (ALP) activities were significantly impaired (p > 0.05) in the tissues with some exceptions among treatment groups relative to the control. The increased stomach, intestinal, and ocular malondialdehyde (MDA) levels (p ≤ 0.05) affirmed the induction of oxidative stress among treatment groups with depleted antioxidant defense system in assessed tissues, but no significant change (p > 0.05) in ocular reduced glutathione (GSH) level was observed, as compared with the control. The tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) levels assessed were significantly elevated (p ≤ 0.05) in the tissues of groups B and D rats with some exceptions among group C rats when compared to the control. The histological alteration characterized by cellular degeneration, oxidative damage, inflammation, and tissue necrosis further affirmed the synergistic impacts with indications of gastritis, retinal dysfunction, and ocular impairment in predisposed rats.
该研究通过让雄性Wistar白化大鼠饮用受污染的水,评估了亚急性镍(Ni)和镉(Cd)暴露对其胃肠系统和眼部系统的生化及组织病理学改变。将四组大鼠,每组六只,分别暴露于未受污染的水(A组作为对照组)、100mg/L的Cd(B组)、100mg/L的Ni(C组)以及100mg/L Cd与Ni的组合(D组)中,持续28天。记录了胃、肠道和眼部的重量,与对照组相比,治疗组的这些重量显著降低(p≤0.05),但与B组和C组大鼠相比,D组大鼠的影响更为显著。所评估的淀粉酶、脂肪酶和碱性磷酸酶(ALP)活性在各组织中均有显著受损(p>0.05),不过治疗组中相对于对照组有一些例外情况。胃、肠道和眼部丙二醛(MDA)水平升高(p≤0.05),这证实了治疗组中存在氧化应激诱导,且所评估组织中的抗氧化防御系统被耗尽,但与对照组相比,眼部还原型谷胱甘肽(GSH)水平未观察到显著变化(p>0.05)。与对照组相比,所评估的肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-10(IL-10)水平在B组和D组大鼠的组织中显著升高(p≤0.05),C组大鼠中有一些例外情况。以细胞变性、氧化损伤、炎症和组织坏死为特征的组织学改变进一步证实了协同作用的影响,表现为易患大鼠出现胃炎、视网膜功能障碍和眼部损伤迹象。