The Role of BNIP3 and Blocked Autophagy Flux in Arsenic-Induced Oxidative Stress-Induced Liver Injury in Rats.

IF 4.3 3区材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC

ACS Applied Electronic Materials Pub Date : 2024-09-01 Epub Date: 2023-12-04 DOI:10.1007/s12011-023-03982-9

Haiyan Zhi, Dingnian Bi, Dan Zheng, Qingyue Lu, Hongling Wang, Yi Wang, Ying Lv, Didong Lou, Yong Hu

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Abstract

Arsenic is a widely distributed environmental toxic substance in nature. Chronic arsenic exposure can cause permanent damage to the liver, resulting in the death of poisoned patients. However, the mechanism of liver damage caused by arsenic poisoning is yet unclear. Here, four different concentrations of sodium arsenite (NaAsO₂) (0 mg/L (control group), 25 mg/L, 50 mg/L, and 100 mg/L group)were established to induce liver injury in rats. Taking this into account, the relationship and potential mechanisms of oxidative stress, Bcl-2/adenovirus E1B-19-kDa-interacting protein 3 (BNIP3), and inhibition of autophagy flux in liver injury caused by arsenic poisoning were studied. The results indicated that long-term exposure to NaAsO₂ could induce oxidative stress, leading to high expression of BNIP3, thereby impaired autophagy flux, and ultimately resulting in liver damage. This research provides an important basis for future research on liver damage caused by chronic arsenic exposure and prevention and treatment with BNIP3 as the target.

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BNIP3和阻断自噬通量在砷诱导氧化应激大鼠肝损伤中的作用

砷是自然界中广泛分布的环境有毒物质。长期接触砷会对肝脏造成永久性损害，导致中毒患者死亡。然而，砷中毒引起肝损伤的机制尚不清楚。本实验采用4种不同浓度的亚砷酸钠(NaAsO2) (0 mg/L(对照组)、25 mg/L、50 mg/L、100 mg/L组)诱导大鼠肝损伤。因此，我们研究了氧化应激、Bcl-2/腺病毒e1b -19- kda相互作用蛋白3 (BNIP3)与自噬通量抑制在砷中毒肝损伤中的关系及潜在机制。结果表明，长期暴露于NaAsO2可诱导氧化应激，导致BNIP3高表达，从而降低自噬通量，最终导致肝脏损伤。本研究为今后以BNIP3为靶点研究慢性砷暴露引起的肝损害及防治提供了重要依据。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

ACS Applied Electronic Materials Multiple-

CiteScore

7.20

自引率

4.30%

发文量

567