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

Klinova, Svetlana V.; Katsnelson, Boris A.; Minigalieva, Ilzira A.; Gerzen, Oksana P.; Балакин, А. А.; Lisin, Ruslan V.; Butova, Xenia; Nabiev, Salavat R.; Lookin, Oleg; Katsnelson, Leonid B.; Privalova, Larisa I.; Kuznetsov, Daniil; Shur, V. Ya.; Шишкина, Е. В.; Makeev, Oleg H.; Valamina, Irene E.; Panov, Vladimir G.; Sutunkova, Marina P.; Никитина, Л. В.; Protsenko, Yuri

doi:10.3390/ijms22073466

Cited by 8 publications

(8 citation statements)

References 52 publications

(26 reference statements)

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“…In both experiments, we modelled moderate subchronic exposure levels and observed statistically significant shifts in a number of rat indices indicating the development of subchronic cadmium poisoning of moderate severity. Toxic effects of cadmium, with a focus on cardiovascular impairments, were described in detail in our previous articles 20,22,23,26,27 . This study is mainly devoted to a qualitative comparison of the effects of CdCl 2 and CdO NPs.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Cardiotoxicity in rats following subchronic exposure to cadmium chloride solution and cadmium oxide nanoparticles

Klinova¹,

Protsenko²,

Minigalieva³

et al. 2022

Public Health Toxicol

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Section: Resultsmentioning

confidence: 99%

“…For genotoxicity assessment, we measured the coefficient of the genomic DNA fragmentation in the nucleated cells of the circulating blood by the random amplified polymorphic DNA (RAPD) analysis as described elsewhere 20 . Twenty-four blood samples (from 6 rats of each group) were analyzed three times.…”

Section: Methodsmentioning

confidence: 99%

Cardiotoxicity in rats following subchronic exposure to cadmium chloride solution and cadmium oxide nanoparticles

Klinova¹,

Protsenko²,

Minigalieva³

et al. 2022

Public Health Toxicol

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“…We observed a rise in the proportion of slow-cycling V3 myosins representing a homodimer of myosin heavy chains (β-MHC 24 % against 8 % in the controls, p <0.05). This change at the molecular level led to a decrease in the sliding velocity of thin filaments over the bed of myosin molecules in experimental rats by 6.1 % (4.6 µm/s against 4.9 µm/s in the controls, p <0.05) [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

“…Myocardial contractility was assessed on isolated multicellular myocardium preparations [ 34 ]. Thin trabeculae and papillary muscles were dissected from the right ventricle of the same heart.…”

Section: Methodsmentioning

confidence: 99%

On the Mechanisms of the Cardiotoxic Effect of Lead Oxide Nanoparticles

Minigaliyeva,

Klinova,

Sutunkova

et al. 2023

Cardiovasc Toxicol

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Lead compounds are one of the most common pollutants of the workplace air and the environment. In the occupational setting, the sources of their emission, including in nanoscale form, are various technological processes associated with lead smelting and handling of non-ferrous metals and their alloys, the production of copper and batteries. Both lead poisoning and lead exposure without obvious signs of poisoning have a detrimental effect on the cardiovascular system. The purpose of this research was to investigate the mechanisms of the cardiotoxic effect of lead oxide nanoparticles (PbO NPs). The toxicological experiment involved male albino rats subchronically exposed to PbO NPs (49.6 ± 16.0 nm in size) instilled intraperitoneally in a suspension. We then assessed post-exposure hematological and biochemical parameters of blood and urine, histological and ultrastructural changes in cardiomyocytes, and non-invasively recorded electrocardiograms and blood pressure parameters in the rodents. Myocardial contractility was studied on isolated preparations of cardiac muscles. We established that PbO NPs induced oxidative stress and damage to the ultrastructure of cardiomyocytes, and decreased efficiency of the contractile function of the myocardium and blood pressure parameters. We also revealed such specific changes in the organism of the exposed rats as anemia, hypoxia, and hypocalcemia. Graphical Abstract

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“…The general and specific toxic effects of Al 2 O 3 , TiO 2 , SiO 2 , PbO, and CdO NPs, as well as cytotoxic effects of CuO and SeO NPs, were discussed in detail in our previous works [ 15 , 30 , 31 , 32 , 33 ]. We have noted that Al 2 O 3 , TiO 2 , SiO 2 , PbO, and CdO NPs exhibit multiple organ toxicity, including certain signs of kidney damage, on which we want to focus in this paper.…”

Section: Introductionmentioning

confidence: 99%

Toxic Kidney Damage in Rats Following Subchronic Intraperitoneal Exposure to Element Oxide Nanoparticles

Ryabova,

Minigalieva,

Sutunkova

et al. 2023

Toxics

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Chronic diseases of the urogenital tract, such as bladder cancer, prostate cancer, reproductive disorders, and nephropathies, can develop under the effects of chemical hazards in the working environment. In this respect, nanosized particles generated as by-products in many industrial processes seem to be particularly dangerous to organs such as the testes and the kidneys. Nephrotoxicity of element oxide particles has been studied in animal experiments with repeated intraperitoneal injections of Al2O3, TiO2, SiO2, PbO, CdO, CuO, and SeO nanoparticles (NPs) in total doses ranging from 4.5 to 45 mg/kg body weight of rats. NPs were synthesized by laser ablation. After cessation of exposure, we measured kidney weight and analyzed selected biochemical parameters in blood and urine, characterizing the state of the excretory system. We also examined histological sections of kidneys and estimated proportions of different cells in imprint smears of this organ. All element oxide NPs under investigation demonstrated a nephrotoxic effect following subchronic exposure. Following the exposure to SeO and SiO2 NPs, we observed a decrease in serum creatinine and urea, respectively. Exposure to Al2O3 NPs caused an increase in urinary creatinine and urea, while changes in total protein were controversial, as it increased under the effect of Al2O3 NPs and was reduced after exposure to CuO NPs. Histomorphological changes in kidneys are associated with desquamation of the epithelium (following the exposure to all NPs except those of Al2O3 and SiO2) and loss of the brush border (following the exposure to all NPs, except those of Al2O3, TiO2, and SiO2). The cytomorphological evaluation showed greater destruction of proximal sections of renal tubules. Compared to the controls, we observed statistically significant alterations in 42.1% (8 of 19) of parameters following the exposure to PbO, CuO, and SeO NPs in 21.1% (4 of 19)—following that, to CdO and Al2O3 NPs—and in 15.8% (3 of 19) and 10.5% (2 of 19) of indicators, following the exposure to TiO2 and SiO2 nanoparticles, respectively. Histomorphological changes in kidneys are associated with desquamation of epithelium and loss of the brush border. The cytomorphological evaluation showed greater destruction of proximal sections of renal tubules. The severity of cyto- and histological structural changes in kidneys depends on the chemical nature of NPs. These alterations are not always consistent with biochemical ones, thus impeding early clinical diagnosis of renal damage. Unambiguous ranking of the NPs examined by the degree of their nephrotoxicity is difficult. Additional studies are necessary to establish key indicators of the nephrotoxic effect, which can facilitate early diagnosis of occupational and nonoccupational nephropathies.

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

Cited by 8 publications

References 52 publications

Cardiotoxicity in rats following subchronic exposure to cadmium chloride solution and cadmium oxide nanoparticles

Cardiotoxicity in rats following subchronic exposure to cadmium chloride solution and cadmium oxide nanoparticles

On the Mechanisms of the Cardiotoxic Effect of Lead Oxide Nanoparticles

Toxic Kidney Damage in Rats Following Subchronic Intraperitoneal Exposure to Element Oxide Nanoparticles

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