Changes in rat myocardium contractility under subchronic intoxication with lead and cadmium salts administered alone or in combination

Protsenko, Yuri; Klinova, Svetlana V.; Gerzen, Oksana P.; Privalova, Larisa I.; Minigalieva, Ilzira A.; Балакин, А. А.; Lookin, Oleg; Lisin, Ruslan V.; Butova, Xenia; Nabiev, Salavat R.; Katsnelson, Leonid B.; Никитина, Л. В.; Katsnelson, Boris A.

doi:10.1016/j.toxrep.2020.03.001

Cited by 22 publications

(11 citation statements)

References 58 publications

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“…In particular, in papillary muscles following exposure to CdO–NP the rate grew and the TTP decreased, while after exposure to PbO–NP the pattern was reversed. We observed similar effects in the experiment with lead and cadmium ions [ 3 ]. In afterloaded contractions, the trabeculae shortening velocity was higher than in the control after exposure to CdO–NP, being significantly different from it after exposure to PbO–NP.…”

Section: Discussionsupporting

confidence: 63%

“…This paper continues our series of publications dealing with the cardiotoxic effects of subchronic intoxication with lead and cadmium salts on the contractility of isolated trabecular and papillary muscle preparations in the isometric and physiological modes and on rat myocardial contractile proteins [ 1 , 2 , 3 , 4 ]. Both lead and cadmium are two of the most common pollutants of the workroom and ambient air associated with metallurgical and some chemical industries being very frequently present together, including in the form of nano-scale particulates.…”

Section: Introductionmentioning

confidence: 77%

“…It is known that undissolved NPs can penetrate into a cell and produce a cytotoxic effect by causing oxidative stress and damage to organelles [ 9 ]. Both metals are well known as multi-vector systemic toxicants, but given the special medico-social significance of cardiovascular morbidity and mortality in the working age population, it is important to understand what evidence could support the widespread suggestion that occupational and environmental exposures to lead and/or cadmium are an essential risk factor in the growth of this pathology [ 1 , 2 , 3 , 4 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

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Cardioinotropic Effects in Subchronic Intoxication of Rats with Lead and/or Cadmium Oxide Nanoparticles

Klinova

Katsnelson

Minigalieva

et al. 2021

IJMS

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Subchronic intoxication was induced in outbred male rats by repeated intraperitoneal injections with lead oxide (PbO) and/or cadmium oxide (CdO) nanoparticles (NPs) 3 times a week during 6 weeks for the purpose of examining its effects on the contractile characteristics of isolated right ventricle trabeculae and papillary muscles in isometric and afterload contractions. Isolated and combined intoxication with these NPs was observed to reduce the mechanical work produced by both types of myocardial preparation. Using the in vitro motility assay, we showed that the sliding velocity of regulated thin filaments drops under both isolated and combined intoxication with CdO–NP and PbO–NP. These results correlate with a shift in the expression of myosin heavy chain (MHC) isoforms towards slowly cycling β–MHC. The type of CdO–NP + PbO–NP combined cardiotoxicity depends on the effect of the toxic impact, the extent of this effect, the ratio of toxicant doses, and the degree of stretching of cardiomyocytes and muscle type studied. Some indices of combined Pb–NP and CdO–NP cardiotoxicity and general toxicity (genotoxicity included) became fully or partly normalized if intoxication developed against background administration of a bioprotective complex.

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Section: Discussionsupporting

confidence: 63%

Section: Introductionmentioning

confidence: 77%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Cardioinotropic Effects in Subchronic Intoxication of Rats with Lead and/or Cadmium Oxide Nanoparticles

Klinova

Katsnelson

Minigalieva

et al. 2021

IJMS

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“…This contributes to the generation of massive ROS; which ultimately causes oxidative stress evidenced in the current study by reduction in the cardiac GSH content and SOD activity in CP treated rats. There has been always a close relation between cardiotoxicity and elevated levels of oxidative stress biomarkers [ [28] , [29] , [30] ]. Oxidative stress initiates myocardial cell damage by stress activation of the ER associated with impaired mitochondrial function, resulting in severe cardiotoxicity [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Rosuvastatin and simvastatin attenuate cisplatin-induced cardiotoxicity via disruption of endoplasmic reticulum stress-mediated apoptotic death in rats: targeting ER-Chaperone GRP78 and Calpain-1 pathways

2020

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Cisplatin (CP) is a powerful antineoplastic chemotherapeutic agent with broad-spectrum properties. Acute and cumulative cardiotoxicity are major limiting factors for CP therapy. Various pathogenic pathways have been suggested to CP-induced cardiotoxicity; oxidative damage, ER stress, and programmed cell death/apoptosis. The present study aimed to assess the signaling mechanisms related to the advantageous effects of rosuvastatin (RSV) and simvastatin (SMV) against CP-related cardiac ER stress dependent apoptotic death in rats. Acute cardiotoxicity was induced by a single dose of CP (10 mg/kg, i.p.) on the 10th day of the experiment. RSV (10 mg/ kg/day) and SMV (10 mg/kg/day) were orally administered for 15 days. CP-treated rats showed significant alterations in electrocardiographic recordings and elevation in serum cardiac function biomarkers; troponin T content, lactate dehydrogenase and creatine kinase-MB levels as well as boost in the cardiac oxidative stress biomarkers. In addition, CP exposure resulted in GRP78 induction; an ER stress and elevation marker at calpain-1 content as well as activation of activated caspase-3 (ACASP3) and caspase-12 were reflected on CP-triggered apoptosis evidenced by elevation in the Bax/Bcl-2 ratio. However, RSV and SMV administration mitigate those adverse CP effects. Statins administration prominently alleviated CP-induced cardiac abnormalities exerting improvement in the ECG pattern and cardiac enzyme biomarkers. Interestingly, statins; RSV and SMV, disrupted CP-induced ER stress and the consequent apoptotic cell death evidenced by downregulation of ER-chaperone GRP78, calpain-1, ACASP3 and caspase-12 as well as decline in the Bax/Bcl-2 ratio. From all the previous findings, it can be suggested that statins namely; RSV and SMV, play protective role against CP-induced cardiac injury by regulating ER stress-mediated apoptotic pathways.

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“…CdCl 2 affected mitochondrial function leading to differential production of ATP in media containing glucose or galactose, like Warburg effect in tumor cells [ 11 ]. Besides, CdCl 2 increased the passive tension of trabecular muscle from the right ventricle in rats [ 12 ]. CdS nanoparticles can cross the blood-brain barrier in dose-dependent manner, without significant toxicity below 0.01 μg /mL [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Promotion of cadmium uptake and cadmium-induced toxicity by the copper transporter CTR1 in HepG2 and ZFL cells

Kwok

Law

et al. 2020

Toxicology Reports

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show abstract

Changes in rat myocardium contractility under subchronic intoxication with lead and cadmium salts administered alone or in combination

Cited by 22 publications

References 58 publications

Cardioinotropic Effects in Subchronic Intoxication of Rats with Lead and/or Cadmium Oxide Nanoparticles

Cardioinotropic Effects in Subchronic Intoxication of Rats with Lead and/or Cadmium Oxide Nanoparticles

Rosuvastatin and simvastatin attenuate cisplatin-induced cardiotoxicity via disruption of endoplasmic reticulum stress-mediated apoptotic death in rats: targeting ER-Chaperone GRP78 and Calpain-1 pathways

Promotion of cadmium uptake and cadmium-induced toxicity by the copper transporter CTR1 in HepG2 and ZFL cells

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