An overview of molecular mechanisms in cadmium toxicity

Đukić-Ćosić, Danijela; Baralić, Katarina; Javorac, Dragana; Djordjevic, Aleksandra Buha; Bulat, Zorica

doi:10.1016/j.cotox.2019.12.002

Cited by 100 publications

(33 citation statements)

References 58 publications

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“…The increase in the activity of GR could be a defense mechanism of the cells, as well as the effect of the increase in the concentration of GSSG being the substrate for GR [ 39 , 57 ]. The Cd-induced drop in the activities of antioxidative enzymes might be, first of all, the result of interactions between this xenobiotic and bioelements incorporated in the active centers of these enzymes: Zn, manganese, and Cu in SOD, selenium in GPx, and Fe in CAT [ 2 , 36 , 58 ].…”

Section: Discussionmentioning

confidence: 99%

“…The elevated levels of LPO, MDA, and 8-isoprostanes noted in the brain tissue in the 5 mg Cd/L group indicate increased lipid peroxidation [ 11 , 15 , 38 , 39 , 44 , 49 , 50 ], whereas the elevated concentration of PC reflects oxidative modifications of proteins [ 39 , 49 , 53 ] in the nervous tissue. The damage to these essential cellular macromolecules may lead to very negative outcomes to the morphological structure and function of neurons [ 40 , 58 ]. Lipid peroxidation is the leading mechanism of Cd toxicity including its neurodegenerative action [ 20 , 21 , 33 , 37 , 40 , 47 , 48 , 49 , 59 ].…”

Section: Discussionmentioning

confidence: 99%

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Enhanced Zinc Intake Protects against Oxidative Stress and Its Consequences in the Brain: A Study in an In Vivo Rat Model of Cadmium Exposure

et al. 2021

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We examined, in a rat model of moderate environmental human exposure to cadmium (Cd), whether the enhanced intake of zinc (Zn) may protect against Cd-caused destroying the oxidative/antioxidative balance and its consequences in the brain. The intoxication with Cd (5 mg/L, 6 months) weakened the enzymatic (superoxide dismutase, glutathione peroxidase, catalase) and non-enzymatic (total thiol groups, reduced glutathione) antioxidative barrier decreasing the total antioxidative status and increased the concentrations of pro-oxidants (hydrogen peroxide, myeloperoxidase) in this organ and its total oxidative status. These resulted in the development of oxidative stress and oxidative modifications of lipids and proteins. The co-administration of Zn (30 and 60 mg/L enhancing this element intake by 79% and 151%, respectively) importantly protected against Cd accumulation in the brain tissue and this xenobiotic-induced development of oxidative stress and oxidative damage to lipids and proteins. Moreover, this bioelement also prevented Cd-mediated oxidative stress evaluated in the serum. The favorable effect of Zn was caused by its independent action and interaction with Cd. Concluding, the enhancement of Zn intake under oral exposure to Cd may prevent the oxidative/antioxidative imbalance and oxidative stress in the brain and thus protect against injury of cellular macromolecules in the nervous system.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Enhanced Zinc Intake Protects against Oxidative Stress and Its Consequences in the Brain: A Study in an In Vivo Rat Model of Cadmium Exposure

et al. 2021

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“…The mode of toxic Cd actions in the organism have been extensively investigated, but still not entirely elucidated, mainly because they may change with the dose and the detailed health status of the exposed subjects. Recent reviews by Đukić-Ćosić et al [ 36 ] and Wallace et al [ 37 ] have summarized the most critical mechanisms of Cd toxicity: changes in gene expression and DNA repair, interference with autophagy and apoptosis pathways, oxidative stress induction, interaction with bioelements, and epigenetic modifications. These mechanisms underlie the possible role of Cd as a metabolic disruptor.…”

Section: Introductionmentioning

confidence: 99%

Emerging Links between Cadmium Exposure and Insulin Resistance: Human, Animal, and Cell Study Data

Buha

Đukić-Ćosić

Ćurčić

et al. 2020

Toxics

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Recent research has helped clarify the role of cadmium (Cd) in various pathological states. We have demonstrated Cd involvement in pancreatic cancer, as well as the bioaccumulation of Cd in the pancreas. Bioaccumulation and increased toxicity suggest that Cd may also be involved in other pancreas-mediated diseases, like diabetes. Cd falls into the category of “hyperglycemic” metals, i.e., metals that increase blood glucose levels, which could be due to increased gluconeogenesis, damage to β-cells leading to reduced insulin production, or insulin resistance at target tissue resulting in a lack of glucose uptake. This review addresses the current evidence for the role of Cd, leading to insulin resistance from human, animal, and in vitro studies. Available data have shown that Cd may affect normal insulin function through multiple pathways. There is evidence that Cd exposure results in the perturbation of the enzymes and modulatory proteins involved in insulin signal transduction at the target tissue and mutations of the insulin receptor. Cd, through well-described mechanisms of oxidative stress, inflammation, and mitochondrial damage, may also alter insulin production in β-cells. More work is necessary to elucidate the mechanisms associated with Cd-mediated insulin resistance.

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“…The most important sources of human exposure to Cd are cigarette smoking and contamination of agricultural soil with Cd-containing phosphate fertilizers and sewage sludge. Several reports have revealed a close association between Cd exposure and the incidence of severe health problems, including cancer, renal dysfunction, liver damage, osteoporosis, and cardiovascular disease [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

“…Unbound Cd ions enter the cells through calcium channels, interfere with mitochondrial function and stimulate the formation of reactive oxygen and nitrogen species (ROS/RNS). Consequently, Cd induces oxidative stress, lysosomal damage, lipid peroxidation, DNA breakage, DNA repair defects, abnormal gene expression, and apoptosis [ 2 , 4 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Inhibitory activity of flaxseed oil against CdCl2 induced liver and kidney damage: Histopathology, genotoxicity, and gene expression study

et al. 2020

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An overview of molecular mechanisms in cadmium toxicity

Cited by 100 publications

References 58 publications

Enhanced Zinc Intake Protects against Oxidative Stress and Its Consequences in the Brain: A Study in an In Vivo Rat Model of Cadmium Exposure

Enhanced Zinc Intake Protects against Oxidative Stress and Its Consequences in the Brain: A Study in an In Vivo Rat Model of Cadmium Exposure

Emerging Links between Cadmium Exposure and Insulin Resistance: Human, Animal, and Cell Study Data

Inhibitory activity of flaxseed oil against CdCl2 induced liver and kidney damage: Histopathology, genotoxicity, and gene expression study

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