Oxidative Damage to BV2 Cells by Trichloroacetic Acid: Protective Role of Boron <i>via</i> the p53 Pathway.

Chong Wang; Wei Huang; Li LI; Chao Wang; Ying Shi; Song Tang; Wen GU; Yong Jun XU; Li Xia Zhang; Ming Zhang; Lian Duan; Kang Feng Zhao

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Oxidative Damage to BV2 Cells by Trichloroacetic Acid: Protective Role of Boron via the p53 Pathway.

Author: Chong WANG ¹ ; Wei HUANG ² ; Li LI ¹ ; Chao WANG ¹ ; Ying SHI ¹ ; Song TANG ¹ ; Wen GU ¹ ; Yong Jun XU ¹ ; Li Xia ZHANG ¹ ; Ming ZHANG ¹ ; Lian DUAN ¹ ; Kang Feng ZHAO ¹
Author Information

1. China CDC Key Laboratory of Environment and Population Health.
2. The Afffiliated Shunde Hospital of Guangzhou Medical University, Foshan 528315, Guangzhou, China.
Publication Type:Letter
Keywords: Boron; Cell apoptotic pathway; Neurotoxicity; Oxidative damage; Trichloroacetic acid
MeSH: Animals; Apoptosis; Boron/toxicity*; Mice; Oxidative Stress; Reactive Oxygen Species/metabolism*; Trichloroacetic Acid/toxicity*; Tumor Suppressor Protein p53/metabolism*
From: Biomedical and Environmental Sciences 2022;35(7):657-662
CountryChina
Language:English
Abstract: This study aimed to investigate the neurotoxicity induced by trichloroacetic acid (TCA) and the possible protective mechanisms of boron (B). Mouse BV2 cells were treated with TCA (0, 0.39, 0.78, 1.56, 3.12, 6.25, or 12.5 mmol/L) and B (0, 7.8, 15.6, 31.25, 62.5, 125, 500, or 1,000 mmol/L) for 3 h and 24 h, respectively. Then, reactive oxygen species, and supernatant proinflammatory cytokine and protein levels were analyzed after 24 h of combined exposure. Beyond the dose-dependent decrease in the cellular viability, it clearly increased after B supplementation ( P < 0.05). Moreover, B decreased oxidative damage, and significantly down-regulated IL-6 levels and up-regulated TNF-β production ( P < 0.05). B also decreased apoptosis via the p53 pathway. The present findings indicated that TCA may induce oxidative damage, whereas B mitigates these adverse effects by decreasing cell apoptosis.