Effects of molybdenum and cadmium on the oxidative damage and kidney apoptosis in Duck

Shi, Lele; Luo, Junrong; Liu, Ping; Wang, Tiancheng; Hu, Guoliang; Zhang, Caiying

doi:10.1016/j.ecoenv.2017.07.006

Cited by 50 publications

(18 citation statements)

References 52 publications

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“…ROS-induced damage results in cytotoxicity through mitochondrial damage and promotion of apoptosis (Jeng and Swanson 2006). The observations are in agreement with previous investigations of one of us (SS) and other investigations in duck renal tubular epithelial cells demonstrating the induction of oxidative stress by tungstate and molybdate in various organs such as the kidneys and the liver, overwhelming the cellular antioxidant defense (Sachdeva et al 2013;Shi et al 2017;Wang et al 2020;Zhang et al 2021).…”

Section: Discussionsupporting

confidence: 90%

Comparative outcomes of exposing human liver and kidney cell lines to tungstate and molybdate

Sachdeva

Maret

2021

Toxicology Mechanisms and Methods

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Tungsten has no known function in humans and is a relatively new contaminant, whereas molybdenum, its congener in the periodic table, is a nutritionally essential element. In addition to early studies on molybdosis in ruminants, their toxic effects in the form of tungstate and molybdate have been addressed primarily in rodents and are predominantly mediated by inducing oxidative stress in various tissues. The purpose of this study was to evaluate the differences between tungstate and molybdate in human liver (HepG2) and kidney (HEK293) cell lines in terms of retention in cells, effect on reactive oxygen species, and activities of xanthine oxidase and phosphatases. The cell lines were exposed to tungstate or molybdate (1 mM to 10 mM) for 24 h, lysed and analyzed for the above biochemical parameters. Despite the chemical similarity of the two anions, cell-specific differential effects were observed. At all concentrations, tungstate was retained more in HEK293 cells while molybdate was retained more in HepG2 cells. HepG2 cells were more sensitive to tungstate than molybdate, showing reduced viability at concentrations as low as 10 mM. Exposure to either anion resulted in the inhibition of protein tyrosine phosphatases at 1 mM and an increased production of reactive oxygen species (ROS) at 100 mM despite their inhibition of the ROS-producing molybdenum enzyme xanthine oxidase. In conclusion, the results indicate that excess of nutritionally essential molybdate or non-essential tungstate causes toxicity by affecting ROS-and phosphorylation-dependent signaling pathways and ensuing gene expression.

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Section: Discussionsupporting

confidence: 90%

Comparative outcomes of exposing human liver and kidney cell lines to tungstate and molybdate

Sachdeva

Maret

2021

Toxicology Mechanisms and Methods

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“…Cadmium induces oxidative stress, this nephron segment is sensitive to damage by oxidative stress [12,14,15]. Some research suggests that Cd induce kidney damage and dysfunction, along with autophagy, both in vivo and in vitro [16,17]. but the molecular mechanisms involved in the cell damage from oxidative stress in cadmium-induced chronic kidney disease are not well understood [18].…”

Section: Am J Biomed Sci and Resmentioning

confidence: 99%

Microarray profiling of long noncoding RNAs and mRNA expression in the kidney of rats damaged by cadmium

Huang

2020

AJBSR

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“…31 A similar synergy also exists between molybdenum and cadmium where kidney antioxidant indices such as glutathione reductase (GR) and ceruloplasmin reduced significantly in co-metal treated groups compared to the single metal treated groups. 32 Similarly, comparing the nephrotoxicity of lead and cadmium, co-exposure to the individual metals caused a more severe decline in renal function. 33 Heavy metal-induced diseases Heavy metal intoxication usually leads to the depletion of cellular antioxidants and a subsequent increase in the generation of excessive ROS leading primarily to oxidative stress.…”

Section: Effect Of Co-exposurementioning

confidence: 99%

Untitled

2020

TJNPR

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contaminants in the environmental systems are the heavy metals which gain access into our environment through natural and human activities such as soil erosion and runoffs , mining and rock weathering, indiscriminate disposal of industrial effluents, sewage discharge, unguided use of pesticides, etc. 1 Although some of these metals are "essential", however, above their permissible limits, such metals become harmful to the body. The WHO permissible limit for cadmium, chromium, copper, lead, manganese and nickel in drinking water are 0.003, 0.05, 2.00, 0.01, 0.50, and 0.02 mg/L, respectively. 2 Above these levels, these metals are no longer beneficial. When aquatic animals ingest heavy metal-contaminated water, they naturally bio-accumulate the metals. Similarly, when plants are irrigated with such water, heavy metal accumulation occurs. The eventual consumption of these is dangerous as it consequently leads to the development of various life-threatening diseases such as cancer and organ damage among others. The threat of heavy metal poisoning is higher for people in rural areas. Particularly, people in neglected parts of developing nations are more prone to such poisoning because of ignorance and lack of potable water supply. 3

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Effects of molybdenum and cadmium on the oxidative damage and kidney apoptosis in Duck

Cited by 50 publications

References 52 publications

Comparative outcomes of exposing human liver and kidney cell lines to tungstate and molybdate

Comparative outcomes of exposing human liver and kidney cell lines to tungstate and molybdate

Microarray profiling of long noncoding RNAs and mRNA expression in the kidney of rats damaged by cadmium

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