Impairment of cell and plasma redox state in subjects professionally exposed to chromium

Mattia, G. De; Bravi, M.; Laurenti, O.; Luca, Ottavia De; Palmeri, Alessandro; Sabatucci, A; Mendico, Gino; Ghiselli, Andrea

doi:10.1002/ajim.20044

Cited by 82 publications

(39 citation statements)

References 27 publications

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“…Additional adenine attenuated ATP depletion, reduced the percentage of PS-exposing cells, and maintained normal RBCs morphology and volume, thereby suggesting that the intracellular ATP level is important in Cr 6+ -induced eryptosis. According to previous reports, increased ROS may be a major mechanism mediating Cr 6+ -induced injury in RBCs and other karyocytes [14,46,47] and increased ROS levels are closely related to eryptosis [48]. We also found that Cr 6+ exposure significantly increased RBCs ROS levels and PS-exposing cells.…”

Section: Discussionsupporting

confidence: 80%

Involvement of Calcium, Reactive Oxygen Species, and ATP in Hexavalent Chromium-Induced Damage in Red Blood Cells

Zhang

Xiang

Ran

et al. 2014

Cell Physiol Biochem

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Aim: The aim of this study was to investigate the mechanisms of Cr⁶⁺-induced red blood cells (RBCs) damage. Methods: The effect of Cr⁶⁺ exposure on RBCs was evaluated by hemolytic rate and blood gas assays. After exposure to 20 μM Cr⁶⁺, the percentage of phosphatidylserine (PS)-exposing cells, intracellular Ca²⁺, reactive oxygen species (ROS), and ATP levels were evaluated, and cell morphology was observed. RBCs were exposed to Cr⁶⁺ in different Ringer solutions to investigate the role of changes of Ca²⁺, ROS, and ATP levels in eryptosis and morphology. Results: The Cr⁶⁺-induced damage of RBCs was dose-dependent. After a 6 h incubation with Cr⁶⁺, RBCs exhibited significant Ca²⁺ influx, ROS increase, ATP depletion, and PS exposure, but displayed no obvious change in morphology at this time point. After 24 h Cr⁶⁺ exposure, the RBCs decreased in size, appeared to be spike-like, and had decreased forward scatter. Inhibition of Ca²⁺ influx attenuated PS-exposure caused by 6 h Cr⁶⁺ exposure, but did not prevent 24 h Cr⁶⁺ exposure-induced morphological change in RBCs. Inhibition of rapid ATP consumption using adenine significantly ameliorated Cr⁶⁺-caused PS-exposure at 12 h, 24 h and 48 h, and prevented 24 h Cr⁶⁺ incubation-induced morphological change in RBCs. Conclusion: Cr⁶⁺ can lead to eryptosis. Ca²⁺ influx, increased ROS levels, and rapid ATP consumption are closely related to Cr⁶⁺-induced RBCs damage. Ca²⁺ influx plays an extremely important role in Cr⁶⁺-mediated toxicity.

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Section: Discussionsupporting

confidence: 80%

Involvement of Calcium, Reactive Oxygen Species, and ATP in Hexavalent Chromium-Induced Damage in Red Blood Cells

Zhang

Xiang

Ran

et al. 2014

Cell Physiol Biochem

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“…Any of these species could attack DNA, proteins, and membrane lipids, thereby disrupting cellular integrity and functions [149, 150]. …”

Section: Chromiummentioning

confidence: 99%

Heavy Metal Toxicity and the Environment

Tchounwou

Yedjou

Patlolla

et al. 2012

Experientia Supplementum

4,734

2,809

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Heavy metals are naturally occurring elements that have a high atomic weight and a density at least 5 times greater than that of water. Their multiple industrial, domestic, agricultural, medical and technological applications have led to their wide distribution in the environment; raising concerns over their potential effects on human health and the environment. Their toxicity depends on several factors including the dose, route of exposure, and chemical species, as well as the age, gender, genetics, and nutritional status of exposed individuals. Because of their high degree of toxicity, arsenic, cadmium, chromium, lead, and mercury rank among the priority metals that are of public health significance. These metallic elements are considered systemic toxicants that are known to induce multiple organ damage, even at lower levels of exposure. They are also classified as human carcinogens (known or probable) according to the U.S. Environmental Protection Agency, and the International Agency for Research on Cancer. This review provides an analysis of their environmental occurrence, production and use, potential for human exposure, and molecular mechanisms of toxicity, genotoxicity, and carcinogenicity.

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“…There are numerous occupational-related exposures each year, which have resulted in an increasing public concern about the potential toxic eVects of Cr at ambient level on human (De Mattia et al 2004). Exposure of Cr can be acute or chronic via inhalation and skin contact.…”

Section: Introductionmentioning

confidence: 99%

Renal impairment caused by chronic occupational chromate exposure

Wang

Jia

Zhang

et al. 2010

Int Arch Occup Environ Health

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Impairment of cell and plasma redox state in subjects professionally exposed to chromium

Abstract: This study demonstrated that in humans, an oxidative stress occurs for Cr exposures as low as those considered safe. This oxidative stress appears to be able to affect intracellular and plasmatic antioxidant defense.

Cited by 82 publications

References 27 publications

Involvement of Calcium, Reactive Oxygen Species, and ATP in Hexavalent Chromium-Induced Damage in Red Blood Cells

Involvement of Calcium, Reactive Oxygen Species, and ATP in Hexavalent Chromium-Induced Damage in Red Blood Cells

Heavy Metal Toxicity and the Environment

Renal impairment caused by chronic occupational chromate exposure

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