Effects of vanadium (sodium metavanadate) and aflatoxin-B1 on cytochrome p450 activities, DNA damage and DNA methylation in human liver cell lines

Desaulniers, Daniel; Cummings-Lorbetskie, Cathy; Leingartner, Karen; Xiao, Gong; Zhou, Gu; Parfett, Craig L.J.

doi:10.1016/j.tiv.2020.105036

Cited by 11 publications

(8 citation statements)

References 101 publications

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“…The PMTDI of 1 ng AF/Kg body weight (bw)/day may be used as a guidance value in the risk assessment of AF from food [16]. Moreover, most of the conducted research reported that the toxicity of AFB1 in Caco-2 and HepG2 cells occurs at a dose of 3.0 µg/mL [29,30]. AFB1 has been found to induce oxidative radical formation through the cytochrome-activated P450 enzyme system, generating lipid peroxidation and reducing antioxidant enzyme activity [31], resulting in the carcinogenicity.…”

Section: Introductionmentioning

confidence: 99%

Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1

Chen

Abdallah

Grootaert

et al. 2022

IJMS

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Fumonisin B1 (FB1) and aflatoxin B1 (AFB1) are frequent contaminants of staple foods such as maize. Oral exposure to these toxins poses health hazards by disrupting cellular signaling. However, little is known regarding the multifaced mitochondrial dysfunction-linked toxicity of FB1 and AFB1. Here, we show that after exposure to FB1 and AFB1, mitochondrial respiration significantly decreased by measuring the oxygen consumption rate (OCR), mitochondrial membrane potential (MMP) and reactive oxygen species (ROS). The current work shows that the integrity of mitochondria (MMP and ROS), that is the central component of cell apoptosis, is disrupted by FB1 and AFB1 in undifferentiated Caco-2 and HepG2 cells as in vitro models for human intestine and liver, respectively. It hypothesizes that FB1 and AFB1 could disrupt the mitochondrial electron transport chain (ETC) to induce mitochondrial dysfunction and break the balance of transferring H+ between the mitochondrial inner membrane and mitochondrial matrix, however, the proton leak is not increasing and, as a result, ATP synthesis is blocked. At the sub-toxic exposure of 1.0 µg/mL for 24h, i.e., a viability of 95% in Caco-2 and HepG2 cells, the mitochondrial respiration was, however, stimulated. This suggests that the treated cells could reserve energy for mitochondrial respiration with the exposure of FB1 and AFB1, which could be a survival advantage.

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Section: Introductionmentioning

confidence: 99%

Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1

Chen

Abdallah

Grootaert

et al. 2022

IJMS

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“…Because ROS are increased by vanadium, they should be considered when evaluating vanadium effects on LPO while also recognizing that the direct effects of vanadium may be toxic as well. Some studies have found that vanadium, in the form of vanadate, can cause damage to DNA through DNA scission, phosphorylation inhibition and oxidation of DNA bases [ 151 , 152 , 153 ]. Individuals exposed to vanadium pentoxide through inhalation had greater amounts of DNA base oxidation [ 151 ].…”

Section: Effects Of Vanadium and Lpo On Plasma Membranes Organelles M...mentioning

confidence: 99%

Biological Consequences of Vanadium Effects on Formation of Reactive Oxygen Species and Lipid Peroxidation

Aureliano

Sousa‐Coelho

Dolan

et al. 2023

IJMS

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Lipid peroxidation (LPO), a process that affects human health, can be induced by exposure to vanadium salts and compounds. LPO is often exacerbated by oxidation stress, with some forms of vanadium providing protective effects. The LPO reaction involves the oxidation of the alkene bonds, primarily in polyunsaturated fatty acids, in a chain reaction to form radical and reactive oxygen species (ROS). LPO reactions typically affect cellular membranes through direct effects on membrane structure and function as well as impacting other cellular functions due to increases in ROS. Although LPO effects on mitochondrial function have been studied in detail, other cellular components and organelles are affected. Because vanadium salts and complexes can induce ROS formation both directly and indirectly, the study of LPO arising from increased ROS should include investigations of both processes. This is made more challenging by the range of vanadium species that exist under physiological conditions and the diverse effects of these species. Thus, complex vanadium chemistry requires speciation studies of vanadium to evaluate the direct and indirect effects of the various species that are present during vanadium exposure. Undoubtedly, speciation is important in assessing how vanadium exerts effects in biological systems and is likely the underlying cause for some of the beneficial effects reported in cancerous, diabetic, neurodegenerative conditions and other diseased tissues impacted by LPO processes. Speciation of vanadium, together with investigations of ROS and LPO, should be considered in future biological studies evaluating vanadium effects on the formation of ROS and on LPO in cells, tissues, and organisms as discussed in this review.

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“…It is known that vanadate is possibly carcinogenic to humans. In vitro vanadate can induce DNA strand breaks in human fibroblasts [48], but it was also found that distinct cell lines may respond differently to NaVO 3 , and that its carcinogenic role at low concentrations may result from stimulation of proliferation of tumorigenic cells [49]. V IV OSO 4 was found genotoxic for normal and cancer cells being able to induce DNA damage in lymphocytes (producing DNA single-and double-strand breaks) and in HeLa cancer cells (imposing only single strand breaks).…”

Section: Binding To Dnamentioning

confidence: 99%

“…Many studies reported cleavage/damage of DNA by either vanadium salts [48][49][50][51][52] or complexes [51,[53][54][55][56][57][58][59][60][61][62]. It is known that several transition metals increase the oxidative stress in cells, which for vanadium has been mainly attributed to the generation of hydroxyl radicals by Fenton-like reactions promoted by physiological hydrogen peroxide [54,55].…”

Section: Binding To Dnamentioning

confidence: 99%

Misinterpretations in Evaluating Interactions of Vanadium Complexes with Proteins and Other Biological Targets

Pessoa

Correia

2021

Inorganics

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In aqueous media, VIV- and VV-ions and compounds undergo chemical changes such as hydrolysis, ligand exchange and redox reactions that depend on pH and concentration of the vanadium species, and on the nature of the several components present. In particular, the behaviour of vanadium compounds in biological fluids depends on their environment and on concentration of the many potential ligands present. However, when reporting the biological action of a particular complex, often the possibility of chemical changes occurring has been neglected, and the modifications of the complex added are not taken into account. In this work, we highlight that as soon as most vanadium(IV) and vanadium(V) compounds are dissolved in a biological media, they undergo several types of chemical transformations, and these changes are particularly extensive at the low concentrations normally used in biological experiments. We also emphasize that in case of a biochemical interaction or effect, to determine binding constants or the active species and/or propose mechanisms of action, it is essential to evaluate its speciation in the media where it is acting. This is because the vanadium complex no longer exists in its initial form.

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Effects of vanadium (sodium metavanadate) and aflatoxin-B1 on cytochrome p450 activities, DNA damage and DNA methylation in human liver cell lines

Cited by 11 publications

References 101 publications

Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1

Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1

Biological Consequences of Vanadium Effects on Formation of Reactive Oxygen Species and Lipid Peroxidation

Misinterpretations in Evaluating Interactions of Vanadium Complexes with Proteins and Other Biological Targets

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