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没食子酸对镉镍混合暴露诱导 BALB/c 小鼠肝肾功能毒性的细胞和遗传保护作用。

Cyto and Genoprotective Potential of Tannic Acid Against Cadmium and Nickel Co-exposure Induced Hepato-Renal Toxicity in BALB/c Mice.

机构信息

Cell and Molecular Biology Lab, Department of Zoology, Panjab University, Chandigarh, India, 160014.

School of Basic and Applied Sciences, Maharaja Agrasen University, Solan, Himachal Pradesh, India, 174103.

出版信息

Biol Trace Elem Res. 2024 Dec;202(12):5624-5636. doi: 10.1007/s12011-024-04117-4. Epub 2024 Feb 23.

Abstract

Tannic acid (TA) is a metal chelating polyphenol that plays a crucial role in metal detoxification, but its modulatory role in co-exposure of these heavy metals' exposure needs to be explored. Cadmium (Cd) and nickel (Ni) are inorganic hazardous chemicals in the environment. Humans are prone to be exposed to the co-exposure of Cd and Ni, but the toxicological interactions of these metals are poorly defined. Present study was undertaken to study the preventive role of TA in Cd-Ni co-exposure-evoked hepato-renal toxicity in BALB/c mice. In the current investigation, increased oxidative stress in metal intoxicated groups was confirmed by elevated peroxidation of the lipids and significant lowering of endogenous antioxidant enzymes. Altered hepato-renal serum markers, DNA fragmentation, and histological alterations were also detected in the metal-treated groups. Present study revealed that Cd is a stronger toxicant than Ni and when co-exposure was administered, additive, sub-additive, and detrimental effects were observed. Prophylactic treatment with TA significantly reinstated the levels of lipid peroxidation (LPO), non-enzymatic, and enzymatic antioxidants. Moreover, it also restored the serum biomarker levels, DNA damage, and histoarchitecture of the given tissues. TA due to its metal chelating and anti-oxidative properties exhibited cyto- and genoprotective potential against Cd-Ni co-exposure-induced hepatic and renal injury.

摘要

单宁酸(TA)是一种金属螯合多酚,在金属解毒中起着至关重要的作用,但它在这些重金属共同暴露时的调节作用需要进一步研究。镉(Cd)和镍(Ni)是环境中的无机有害化学物质。人类容易接触到 Cd 和 Ni 的共同暴露,但这些金属的毒理学相互作用尚未得到明确界定。本研究旨在研究 TA 在 BALB/c 小鼠 Cd-Ni 共同暴露诱导的肝肾功能毒性中的预防作用。在本研究中,通过脂质过氧化作用的升高和内源性抗氧化酶的显著降低,证实了金属中毒组的氧化应激增加。在金属处理组中还检测到血清标志物、DNA 片段化和组织学改变的改变。本研究表明,Cd 比 Ni 毒性更强,当进行共同暴露时,观察到了相加、亚相加和有害作用。TA 的预防性治疗显著恢复了脂质过氧化(LPO)、非酶和酶抗氧化剂的水平。此外,它还恢复了血清生物标志物水平、DNA 损伤和给予组织的组织学结构。由于 TA 具有金属螯合和抗氧化特性,因此对 Cd-Ni 共同暴露诱导的肝肾功能损伤表现出细胞和遗传保护潜力。

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