Cadmium-Induced Cytotoxicity: Effects on Mitochondrial Electron Transport Chain

Branca, Jacopo Junio Valerio; Pacini, Alessandra; Gulisano, Massimo; Taddei, Niccolò; Fiorillo, Claudia; Becatti, Matteo

doi:10.3389/fcell.2020.604377

Cited by 69 publications

(39 citation statements)

References 67 publications

(91 reference statements)

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“…Linking TCA cycle and electron transport system, SDH catalyzes the oxidation of succinate to fumarate and plays a central role in mitochondrial metabolism (Jardim-Messeder et al, 2015). It has been well documented that SDH is the target of Cd (Belyaeva, 2018;Branca et al, 2020) because of its richness of reactive sulfhydryl group (Jay et al, 1991). The inhibition of SDH activity in low concentration (9 and 27 μg/L) of Cd-treated clams was in agreement with those in Cd-treated oysters (Ivanina et al, 2008).…”

Section: Non-monotonic Metabolic Responses To CDsupporting

confidence: 59%

Dose-dependent responses of metabolism and tissue injuries in clam Ruditapes philippinarum after subchronic exposure to cadmium

Zhan

Wang

et al. 2021

Science of The Total Environment

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Section: Non-monotonic Metabolic Responses To CDsupporting

confidence: 59%

Dose-dependent responses of metabolism and tissue injuries in clam Ruditapes philippinarum after subchronic exposure to cadmium

Zhan

Wang

et al. 2021

Science of The Total Environment

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“…Alternatively, the process of mitochondrial energy metabolism is also a vulnerable process in external toxic stimulation (Henchcliffe & Beal, 2008). Some studies showed that mitochondrial membrane permeability and electron transport chain (ETC) are the primary targets of Cd induced mitochondrial dysfunction (Branca, Pacini, et al, 2020). Thus, we tested mitochondrial energy metabolism including mitochondria stress test and glycolysis rate analysis using seahorse XFp Extracellular Flux Analyzer.…”

Section: Discussionmentioning

confidence: 99%

Cadmium inhibits neural stem/progenitor cells proliferation via MitoROS‐dependent AKT/GSK‐3β/β‐catenin signaling pathway

Luo

Song

Xiong

et al. 2021

J of Applied Toxicology

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Cadmium (Cd) is a toxic heavy metal widely found in the environment. Cd is also a potential neurotoxicant, and its exposure is associated with impairment of cognitive function. However, the underlying mechanisms by which Cd induces neurotoxicity are unclear. In this study, we investigated the in vitro effect of Cd on primary murine neural stem/progenitor cells (mNS/PCs) isolated from the subventricular zone. Our results show that Cd exposure leads to mNS/PCs G1/S arrest, promotes cell apoptosis, and inhibits cell proliferation. In addition, Cd increases intracellular and mitochondrial reactive oxygen species (ROS) that activates mitochondrial oxidative stress, decreases ATP production, and increases mitochondrial proton leak and glycolysis rate in a dose‐dependent manner. Furthermore, Cd exposure decreases phosphorylation of protein kinase B (AKT) and glycogen synthase kinase‐3 beta (GSK3β) in mNS/PCs. In addition, pretreatment mNS/PCs with MitoTEMPO, a mitochondrial‐targeted antioxidant, improves mitochondrial morphology and functions and attenuates Cd‐induced inhibition of mNS/PCs proliferation. It also effectively reverses Cd‐induced changes of phosphorylation of AKT and the expression of β‐catenin and its downstream genes. Taken together, our data suggested that AKT/GSK3β/β‐catenin signaling pathway is involved in Cd‐induced mNS/PCs proliferation inhibition via MitoROS‐dependent pattern.

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“…Occupational exposure usually occurs in industries involving mining, batteries, pigments, coatings, electroplating and plastic stabilizers. Sources of cadmium exposure include plastic toys, battery, paints, ceramics, contaminated water, air, soil, food, fertilizers, and cigarette smoke [9,10].…”

Section: Introductionmentioning

confidence: 99%

Effects of Cadmium Exposure on Leydig Cells and Blood Vessels in Mouse Testis

Yang

Chen

et al. 2022

IJERPH

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Environmental exposure to cadmium (Cd) contributes to a decline in the quality of human semen. Although the testis is sensitive to Cd exposure, the mechanism underlying how cadmium affects the testis remains to be defined. In this study, male mice were treated with intraperitoneal injections of 0, 0.5, 1.5 and 2.5 mg CdCl2/kg/day for 10 days, respectively. Both the testicular weight and the 3β-HSD activity of Leydig cells were significantly reduced with the administration of 2.5 mg CdCl2/kg/day. The height of endothelial cells in the interstitial blood vessels significantly increased with the use of 2.5 mg CdCl2/kg/day compared with the control. Western blot data showed that the protein levels of CD31, αSMA, caveolin and Ng2 increased with cadmium exposure, and this increase was particularly significant with the administration of 2.5 mg CdCl2/kg/day. CD31, αSMA, caveolin and Ng2 are related to angiogenesis. Based on our data, cadmium exposure may stimulate the proliferation of the mural cells and endothelial cells of blood vessels, which may lead to abnormal function of the testis.

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Cadmium-Induced Cytotoxicity: Effects on Mitochondrial Electron Transport Chain

Cited by 69 publications

References 67 publications

Dose-dependent responses of metabolism and tissue injuries in clam Ruditapes philippinarum after subchronic exposure to cadmium

Dose-dependent responses of metabolism and tissue injuries in clam Ruditapes philippinarum after subchronic exposure to cadmium

Cadmium inhibits neural stem/progenitor cells proliferation via MitoROS‐dependent AKT/GSK‐3β/β‐catenin signaling pathway

Effects of Cadmium Exposure on Leydig Cells and Blood Vessels in Mouse Testis

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