Corrigendum to “Evaluation of in vivo and in vitro toxicological and genotoxic potential of aluminum chloride” [Chemosphere 175 (2017), 130–137]

Since the mid-1970s there have been many reports that purport to implicate aluminium in the etiology of neurodegenerative disease. After several decades of research, the role of aluminium in such disease remains controversial and is not the subject of this review. However, if aluminium is implicated in such disease then it follows that there must be a toxicological mechanism, or mode of action, and many researchers have investigated various potential mechanisms including the involvement of oxidative damage, cytotoxicity, and genotoxicity. This paper reviews many of the publications of studies using various salts of aluminium and various genotoxicity endpoints, both in vitro and in vivo, with a focus on oxidative damage. The conclusion of this review is that the majority, if not all, of the publications that report positive results have serious technical flaws and/or implausible findings, and consequently should contribute little or no weight to a weight of evidence (WoE) argument. There are many high quality, GLP compliant genotoxicity studies, that follow relevant OECD test guidelines and the ECHA integrated mutagenicity testing strategy, on several salts of aluminium; all demonstrate clear negative results for both in vitro and in vivo genotoxicity. In addition, the claim for an oxidative mode of action for aluminium can be shown to be spurious. This review concludes that there are no reliable studies that demonstrate a potential for genotoxicity, or oxidative mode of action, for aluminium.

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Aluminum induces oxidative damage in Saccharomyces cerevisiae

Chen

Zhu

Fang

et al. 2020

Can. J. Microbiol.

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The mechanism of aluminum toxicity was studied in the model cells of Saccharomyces cerevisiae. Cell growth of yeast was inhibited by aluminum. The spot assay showed that the detoxification mechanism of yeast cells to aluminum was different from that of heavy metal cadmium. After treatment with aluminum, intracellular levels of reactive oxygen species, carbonyl protein and thiobarbituric acid reactive substances were dramatically increased. Meanwhile, the percentage of propidium iodide permeable cells treated with aluminum was augmented significantly. These data demonstrated that aluminum toxicity was attributed to oxidative stress in yeast and it induced oxidative damage by causing lipid peroxidation, injuring cell membrane integrity. Moreover, aluminum triggered the antioxidant defense system in the cells. Glutathione levels were found to be decreased, while activities of superoxide dismutase and catalase were increased after treatment with aluminum. Additionally, an oxidative stress-related mutation sensitivity assay showed that aluminum-induced yeast oxidative stress was closely related to glutathione. These data demonstrated that the oxidative damage caused by aluminum was different from that of hydrogen peroxide in yeast. Aluminum could cause DNA damage, and aluminum toxicity was associated with sulfhydryl groups, such as glutathione, while it was independent of YAP1.

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Corrigendum to “Evaluation of in vivo and in vitro toxicological and genotoxic potential of aluminum chloride” [Chemosphere 175 (2017), 130–137]

Cited by 3 publications

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Genotoxic properties of materials used for endoprostheses: Experimental and human data

Genotoxic properties of materials used for endoprostheses: Experimental and human data

Critical review of the publications on the genotoxicology of aluminium salts: 1990–2018

Aluminum induces oxidative damage in Saccharomyces cerevisiae

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