Puerarin alleviates cadmium-induced mitochondrial mass decrease by inhibiting PINK1–Parkin and Nix-mediated mitophagy in rat cortical neurons

Wen, Sicheng; Wang, Li; Wang, Tao; Xu, Mingchang; Zhang, Wenhua; Song, Ruilong; Zou, Hui; Gu, Jianhong; Bian, Jianchun; Yuan, Yan; Liu, Zongping

doi:10.1016/j.ecoenv.2021.113127

Cited by 12 publications

(7 citation statements)

References 44 publications

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“…WEN [43] found that expression levels of the mitochondrial marker proteins HSP60 and COXIV were significantly reduced after the Cd treatment of rat cerebral cortical neurons for 12 h and 24 h. The mitochondrial ultrastructure showed obvious damage, forming a large number of mitochondrial auto-phagosomes, which suggests that Cd removes neuronal mitochondria by activating mitochondrial autophagy. This further demonstrates that Cd could promote mitochondrial autophagy and damage the mitochondrial structure by lowering the mitochondrial membrane potential, thus promoting apoptosis and causing the liver to lose its normal physiological function.…”

Section: Discussionmentioning

confidence: 99%

Tetramethylpyrazine Antagonizes the Subchronic Cadmium Exposure-Induced Oxidative Damage in Mouse Livers via the Nrf2/HO-1 Pathway

Hu,

Zhao,

Guo

et al. 2024

Molecules

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Hepatic oxidative stress is an important mechanism of Cd-induced hepatotoxicity, and it is ameliorated by TMP. However, this underlying mechanism remains to be elucidated. To investigate the mechanism of the protective effect of TMP on liver injuries in mice induced by subchronic cadmium exposure, 60 healthy male ICR mice were randomly divided into five groups of 12 mice each, namely, control (CON), Cd (2 mg/kg of CdCl2), Cd + 100 mg/kg of TMP, Cd + 150 mg/kg of TMP, and Cd + 200 mg/kg of TMP, and were acclimatized and fed for 7 d. The five groups of mice were gavaged for 28 consecutive days with a maximum dose of 0.2 mL/10 g/day. Except for the control group, all groups were given fluoride (35 mg/kg) by an intraperitoneal injection on the last day of the experiment. The results of this study show that compared with the Cd group, TMP attenuated CdCl2-induced pathological changes in the liver and improved the ultrastructure of liver cells, and TMP significantly decreased the MDA level (p < 0.05) and increased the levels of T-AOC, T-SOD, and GSH (p < 0.05). The results of mRNA detection show that TMP significantly increased the levels of Nrf2 in the liver compared with the Cd group as well as the HO-1 and mRNA expression levels in the liver (p < 0.05). In conclusion, TMP could inhibit oxidative stress and attenuate Cd group-induced liver injuries by activating the Nrf2 pathway.

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Section: Discussionmentioning

confidence: 99%

Tetramethylpyrazine Antagonizes the Subchronic Cadmium Exposure-Induced Oxidative Damage in Mouse Livers via the Nrf2/HO-1 Pathway

Hu,

Zhao,

Guo

et al. 2024

Molecules

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“…[ 128 ] This aligns with our observations that Cd triggers PINK1/Parkin‐mediated mitophagy in rat cerebral cortical neurons. [ 129 ] Nevertheless, further investigation is required to elucidate the role of Cd‐induced mitophagy in the brain completely. Zhang et al [ 130 ] revealed that PINK1/Parkin‐mediated mitophagy can serve as a protective mechanism against cisplatin‐related neurotoxicity.…”

Section: And Autophagy In the Cnsmentioning

confidence: 99%

Cadmium neurotoxicity and therapeutic strategies

Wen,

Wang

2024

J Biochem & Molecular Tox

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Cadmium (Cd) is a multitarget, carcinogenic, nonessential environmental pollutant. Due to its toxic effects at very low concentrations, lengthy biological half‐life, and low excretion rate, exposure to Cd carries a concern. Prolonged exposure to Cd causes severe injury to the nervous system of both humans and animals. Nevertheless, the precise mechanisms responsible for the neurotoxic effects of Cd have yet to be fully elucidated. The accurate chemical mechanism potentially entails the destruction of metal‐ion homeostasis, inducing oxidative stress, apoptosis, and autophagy. Here we review the evidence of the neurotoxic effects of Cd and corresponding strategies to protect against Cd‐induced central nervous system injury.

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“…According to Yan et al, cadmium exposure (5, 10, and 20 μM) induced cortical neuron apoptosis, which is mediated by oxidative stress and mitochondrial dysfunction [ 120 ]. Wen et al [ 121 , 122 ] further found that puerarin protects against cadmium-induced (10 μM) neurotoxicity by alleviating mitochondrial damage, and inhibiting mitophagy-mediated mitochondrial mass decrease. In vivo, their results demonstrated that puerarin inhibited cadmium-induced neurotoxicity by alleviating oxidative stress and apoptosis in rat cerebral cortical neurons.…”

Section: The Toxicity Of Cadmium Toward the Kidney Liver Bone And Brainmentioning

confidence: 99%

The Effect of Oxidative Stress-Induced Autophagy by Cadmium Exposure in Kidney, Liver, and Bone Damage, and Neurotoxicity

Yue

et al. 2022

IJMS

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Environmental and occupational exposure to cadmium has been shown to induce kidney damage, liver injury, neurodegenerative disease, and osteoporosis. However, the mechanism by which cadmium induces autophagy in these diseases remains unclear. Studies have shown that cadmium is an effective inducer of oxidative stress, DNA damage, ER stress, and autophagy, which are thought to be adaptive stress responses that allow cells exposed to cadmium to survive in an adverse environment. However, excessive stress will cause tissue damage by inducing apoptosis, pyroptosis, and ferroptosis. Evidently, oxidative stress-induced autophagy plays different roles in low- or high-dose cadmium exposure-induced cell damage, either causing apoptosis, pyroptosis, and ferroptosis or inducing cell survival. Meanwhile, different cell types have different sensitivities to cadmium, which ultimately determines the fate of the cell. In this review, we provided a detailed survey of the current literature on autophagy in cadmium-induced tissue damage. A better understanding of the complex regulation of cell death by autophagy might contribute to the development of novel preventive and therapeutic strategies to treat acute and chronic cadmium toxicity.

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Puerarin alleviates cadmium-induced mitochondrial mass decrease by inhibiting PINK1–Parkin and Nix-mediated mitophagy in rat cortical neurons

Cited by 12 publications

References 44 publications

Tetramethylpyrazine Antagonizes the Subchronic Cadmium Exposure-Induced Oxidative Damage in Mouse Livers via the Nrf2/HO-1 Pathway

Tetramethylpyrazine Antagonizes the Subchronic Cadmium Exposure-Induced Oxidative Damage in Mouse Livers via the Nrf2/HO-1 Pathway

Cadmium neurotoxicity and therapeutic strategies

The Effect of Oxidative Stress-Induced Autophagy by Cadmium Exposure in Kidney, Liver, and Bone Damage, and Neurotoxicity

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