Disruption of mitochondrial redox homeostasis as a mechanism of antimony-induced reactive oxygen species and cytotoxicity

Su, Liling; Fang, Wenpan; Zhao, Xinyuan; Zhu, Longtao; Gao, Lan; Chen, Guangdi

doi:10.1016/j.ecoenv.2022.113519

Cited by 11 publications

(3 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mitochondrial and cell research. Experiments with Sb 3+ -treated mitochondria isolated from A549 cells showed an increase in SOD activity and a decrease in CI and CIII activities, glutathione peroxidase, glutathione reductase, and thioredoxin reductase [307]. The compounds and complexes of pentavalent and trivalent antimony with potassium antimonyl tartrate are used to treat leishmaniasis caused by protozoan parasites [308][309][310].…”

Section: Al(iii) Ga(iii) and In(iiimentioning

confidence: 99%

“…The compounds and complexes of pentavalent and trivalent antimony with potassium antimonyl tartrate are used to treat leishmaniasis caused by protozoan parasites [308][309][310]. Sb(III) (Sb 2 O 3 and SbCl 3 ) induced apoptosis and cell viability loss; an increase in ROS production; and a decrease in the cytoplasm glutathione level, ∆Ψ mito , and ATP content in human lung adenocarcinoma A549 cells, human embryonic kidney HEK-293 cells, and CCRF-CEM line cells [307,311,312]. Potassium antimonyl tartrate (K 2 [SbC 2 H 2 (O) 2 (COO) 2 ] 2 ) and As 2 O 3 had similar effects in experiments with human lymphoid tumoral cells and human myeloid leukemic HL60 cells [313,314].…”

Section: Al(iii) Ga(iii) and In(iiimentioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

Korotkov

2023

IJMS

View full text Add to dashboard Cite

This review analyzes the causes and consequences of apoptosis resulting from oxidative stress that occurs in mitochondria and cells exposed to the toxic effects of different-valence heavy metals (Ag+, Tl+, Hg2+, Cd2+, Pb2+, Al3+, Ga3+, In3+, As3+, Sb3+, Cr6+, and U6+). The problems of the relationship between the integration of these toxic metals into molecular mechanisms with the subsequent development of pathophysiological processes and the appearance of diseases caused by the accumulation of these metals in the body are also addressed in this review. Such apoptosis is characterized by a reduction in cell viability, the activation of caspase-3 and caspase-9, the expression of pro-apoptotic genes (Bax and Bcl-2), and the activation of protein kinases (ERK, JNK, p53, and p38) by mitogens. Moreover, the oxidative stress manifests as the mitochondrial permeability transition pore (MPTP) opening, mitochondrial swelling, an increase in the production of reactive oxygen species (ROS) and H2O2, lipid peroxidation, cytochrome c release, a decline in the inner mitochondrial membrane potential (ΔΨmito), a decrease in ATP synthesis, and reduced glutathione and oxygen consumption as well as cytoplasm and matrix calcium overload due to Ca2+ release from the endoplasmic reticulum (ER). The apoptosis and respiratory dysfunction induced by these metals are discussed regarding their interaction with cellular and mitochondrial thiol groups and Fe2+ metabolism disturbance. Similarities and differences in the toxic effects of Tl+ from those of other heavy metals under review are discussed. Similarities may be due to the increase in the cytoplasmic calcium concentration induced by Tl+ and these metals. One difference discussed is the failure to decrease Tl+ toxicity through metallothionein-dependent mechanisms. Another difference could be the decrease in reduced glutathione in the matrix due to the reversible oxidation of Tl+ to Tl3+ near the centers of ROS generation in the respiratory chain. The latter may explain why thallium toxicity to humans turned out to be higher than the toxicity of mercury, lead, cadmium, copper, and zinc.

show abstract

Section: Al(iii) Ga(iii) and In(iiimentioning

confidence: 99%

Section: Al(iii) Ga(iii) and In(iiimentioning

confidence: 99%

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

Korotkov

2023

IJMS

View full text Add to dashboard Cite

show abstract

“…However, in our study, we observed no changes regarding the induction of apoptosis or mitophagy in CRIF1-deficient MCF-7 cells, whereas a significant percentage of these cells exhibited G0/G1 phase arrest during the cell cycle. The disruption of mitochondrial homeostasis (e.g., mitochondrial stress, dynamics, and function) mediates deceleration of the cell cycle, in conjunction with elevated levels of ROS and DNA damage [ 32 , 33 , 34 ]. Therefore, CRIF1 deficiency destroyed mitochondrial homeostasis and caused a significant inhibition of cell growth.…”

Section: Discussionmentioning

confidence: 99%

CRIF1 siRNA-Encapsulated PLGA Nanoparticles Suppress Tumor Growth in MCF-7 Human Breast Cancer Cells

Piao

Lee

Kim

et al. 2023

IJMS

View full text Add to dashboard Cite

Mitochondrial oxidative phosphorylation (OXPHOS) system dysfunction in cancer cells has been exploited as a target for anti-cancer therapeutic intervention. The downregulation of CR6-interacting factor 1 (CRIF1), an essential mito-ribosomal factor, can impair mitochondrial function in various cell types. In this study, we investigated whether CRIF1 deficiency induced by siRNA and siRNA nanoparticles could suppress MCF-7 breast cancer growth and tumor development, respectively. Our results showed that CRIF1 silencing decreased the assembly of mitochondrial OXPHOS complexes I and II, which induced mitochondrial dysfunction, mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential depolarization, and excessive mitochondrial fission. CRIF1 inhibition reduced p53-induced glycolysis and apoptosis regulator (TIGAR) expression, as well as NADPH synthesis, leading to additional increases in ROS production. The downregulation of CRIF1 suppressed cell proliferation and inhibited cell migration through the induction of G0/G1 phase cell cycle arrest in MCF-7 breast cancer cells. Similarly, the intratumoral injection of CRIF1 siRNA-encapsulated PLGA nanoparticles inhibited tumor growth, downregulated the assembly of mitochondrial OXPHOS complexes I and II, and induced the expression of cell cycle protein markers (p53, p21, and p16) in MCF-7 xenograft mice. Thus, the inhibition of mitochondrial OXPHOS protein synthesis through CRIF1 deletion destroyed mitochondrial function, leading to elevated ROS levels and inducing antitumor effects in MCF-7 cells.

show abstract

Associations of personal PM2.5-bound heavy metals and heavy metal mixture with lung function: Results from a panel study in Chinese urban residents

Zhang,

Hu,

Wang

et al. 2024

Chemosphere

View full text Add to dashboard Cite

Disruption of mitochondrial redox homeostasis as a mechanism of antimony-induced reactive oxygen species and cytotoxicity

Cited by 11 publications

References 39 publications

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

CRIF1 siRNA-Encapsulated PLGA Nanoparticles Suppress Tumor Growth in MCF-7 Human Breast Cancer Cells

Associations of personal PM2.5-bound heavy metals and heavy metal mixture with lung function: Results from a panel study in Chinese urban residents

Contact Info

Product

Resources

About