Thorium inhibits human respiratory chain complex IV (cytochrome c oxidase)

Yu, Libing; Lin, Zhaozhu; Cheng, Xuedan; Chu, Jian; Li, Xijian; Chen, Chun; Zhu, Tinghua; Li, Wenjing; Lin, Wei; Tang, Wei

doi:10.1016/j.jhazmat.2021.127546

Cited by 12 publications

(3 citation statements)

References 51 publications

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“…CIV, also known as cyto-c oxidase, is a multisubunit protein complex that facilitates the transfer of electrons from the respiratory chain to oxygen molecules via cytochromes [ 125 , 126 ]. As humans age, mitochondrial mutations and respiratory chain defects tend to accumulate.…”

Section: Regulation Of the Mrc In Bone Metabolismmentioning

confidence: 99%

The Emerging Role of the Mitochondrial Respiratory Chain in Skeletal Aging

Tao,

Zhu,

Xia

et al. 2023

Aging and disease

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Maintenance of mitochondrial homeostasis is crucial for ensuring healthy mitochondria and normal cellular function. This process is primarily responsible for regulating processes that include mitochondrial OXPHOS, which generates ATP, as well as mitochondrial oxidative stress, apoptosis, calcium homeostasis, and mitophagy. Bone mesenchymal stem cells express factors that aid in bone formation and vascular growth. Positive regulation of hematopoietic stem cells in the bone marrow affects the differentiation of osteoclasts. Furthermore, the metabolic regulation of cells that play fundamental roles in various regions of the bone, as well as interactions within the bone microenvironment, actively participates in regulating bone integrity and aging. The maintenance of cellular homeostasis is dependent on the regulation of intracellular organelles, thus understanding the impact of mitochondrial functional changes on overall bone metabolism is crucially important. Recent studies have revealed that mitochondrial homeostasis can lead to morphological and functional abnormalities in senescent cells, particularly in the context of bone diseases. Mitochondrial dysfunction in skeletal diseases results in abnormal metabolism of bone-associated cells and a secondary dysregulated microenvironment within bone tissue. This imbalance in the oxidative system and immune disruption in the bone microenvironment ultimately leads to bone dysplasia. In this review, we examine the latest developments in mitochondrial respiratory chain regulation and its impacts on maintenance of bone health. Specifically, we explored whether enhancing mitochondrial function can reduce the occurrence of bone cell deterioration and improve bone metabolism. These findings offer prospects for developing bone remodeling biology strategies to treat age-related degenerative diseases.

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Section: Regulation Of the Mrc In Bone Metabolismmentioning

confidence: 99%

The Emerging Role of the Mitochondrial Respiratory Chain in Skeletal Aging

Tao,

Zhu,

Xia

et al. 2023

Aging and disease

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“…generation, which enhances the effect of H 2 O 2 and other organic peroxides in cells ( 43 ). The majority of O 2 consumed by aerobic organisms is safely reduced to H 2 O in a four-electron transfer reaction catalyzed by the cytochrome oxidase complex IV of the mitochondrial inner membrane respiratory chain ( 44 ). However, a fraction of unused O 2 is involved in other physiological reactions, such as phagocytosis and immune activation.…”

Section: Epigenetics Iron Homeostasis and Rosmentioning

confidence: 99%

Regulators of epigenetic change in ferroptosis‑associated cancer (Review)

Zhu

Wang

et al. 2022

Oncol Rep

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The occurrence of tumors is associated with the upregulation or downregulation of certain genes. The identification of novel tumor therapies has revealed that regulation of tumor cell death can either promote or suppress the occurrence and development of tumors. Iron-dependent lipid free oxygen radical accumulation causes tumor cells to die by ferroptosis, a form of regulated cell death. Multiple mechanisms mediate this mode of cell death, including redox homeostasis, iron metabolism, mitochondrial activity, breakdown of amino acids, lipids and sugars and epigenetic regulatory and disease-associated signaling pathways. The present review discussed epigenetic mechanism of ferroptosis with the aim of providing novel insight for optimization of the effects of antitumor therapy. Contents1. Introduction 2. Epigenetics, iron homeostasis and ROS 3. Mechanisms of ferroptosis in cancer 4. Epigenetic regulation of ferroptosis in cancer 5. Histone modifications and ferroptosis 6. Conclusion

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“…49 Moreover, effects of Th on human proteins viz. hemoglobin, 50 serum albumin, 51 transferrin, 52 cytochrome c oxidase, 53 etc. have also been investigated, which yielded significant insights about its site of interaction.…”

Section: Introductionmentioning

confidence: 99%

Thorium Alters Lung Surfactant Protein Expression in Alveolar Epithelial Cells: In Vitro and In Vivo Investigation

Das,

Ali,

Shetake

et al. 2024

Environ. Sci. Technol.

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Thorium-232 (Th), the most abundant naturally occurring nuclear fuel, has been identified as a sustainable source of energy. In view of its large-scale utilization and human evidence of lung disorders and carcinogenicity, it is imperative to understand the effect of Th exposure on lung cells. The present study investigated the effect of Th-dioxide (1–100 μg/mL, 24–48 h) on expression of surfactant proteins (SPs) (SP-A, SP-B, SP-C, and SP-D, which are essential to maintain lung’s surface tension and host-defense) in human lung cells (WI26 and A549), representative of alveolar cell type-I and type-II, respectively. Results demonstrated the inhibitory effect of Th on transcriptional expression of SP-A, SP-B, and SP-C. However, Th promoted the mRNA expression of SP-D in A549 and reduced its expression in WI26. To a significant extent, the effect of Th on SPs was found to be in accordance with their protein levels. Moreover, Th exposure altered the extracellular release of SP-D/A from A549, which remained unaltered in WI26. Our results suggested the differential role of oxidative stress and ATM and HSP90 signaling in Th-induced alterations of SPs. These effects of Th were found to be consistent in lung tissues of mice exposed to Th aerosols, suggesting a potential role of SPs in Th-associated lung disorders.

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Thorium inhibits human respiratory chain complex IV (cytochrome c oxidase)

Cited by 12 publications

References 51 publications

The Emerging Role of the Mitochondrial Respiratory Chain in Skeletal Aging

The Emerging Role of the Mitochondrial Respiratory Chain in Skeletal Aging

Regulators of epigenetic change in ferroptosis‑associated cancer (Review)

Thorium Alters Lung Surfactant Protein Expression in Alveolar Epithelial Cells: In Vitro and In Vivo Investigation

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