Effects of green tea polyphenols against metal-induced genotoxic damage: underlying mechanistic pathways

Garcia‐Rodriguez, María del Carmen; Hernández-Cortés, Lourdes Montserrat; Mendoza-Núñez, Vı́ctor Manuel; Arenas-Huertero, Francisco

doi:10.1080/10937404.2023.2224119

Cited by 6 publications

(4 citation statements)

References 91 publications

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“…When toxicity impacts erythropoiesis, mechanisms of cell division may be triggered, potentially masking the cytotoxic effect (Krishna & Hayashi, 2000;Tweats et al, 2007). AO/EB analysis revealed a significant rise in the numbers of total apoptotic and early apoptotic cells, as well as nonviable cells, supporting previous reports on the cytotoxicity of Cr(VI) compounds (García-Rodríguez et al, 2013, 2016García-Rodríguez, Hernández-Cortés, et al, 2023;Jomova & Valko, 2011).…”

Section: Apoptosis Necrosis and Cell Viabilitysupporting

confidence: 84%

“…The generation of reactive oxygen species and DNA damage induced by Cr(VI) exposure are considered to play a critical role in cytotoxicity and the initiation of apoptotic signaling pathways (Hu et al, 2017). Investigators demonstrated that Cr(VI) increased the number of apoptotic cells in both in vivo and in vitro mammalian systems (García-Rodríguez et al, 2013, 2016García-Rodríguez, Hernández-Cortés, et al, 2023;Islam et al, 2022). Evidence indicates that apoptosis may play a role in eliminating cells with DNA damage, including micronucleated cells.…”

Section: Apoptosis Necrosis and Cell Viabilitymentioning

confidence: 99%

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A comparative study on chromium‐induced micronuclei assessment in the peripheral blood of Hsd:ICR mice

García‐Rodríguez,

Hernández‐Cortés,

Montaño‐Rodríguez

et al. 2023

J of Applied Toxicology

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This study investigated the genotoxic effects of chromium (Cr) in Hsd:ICR mice, considering factors such as oxidative state, apoptosis, exposure pathway, duration, pregnancy, and transplacental exposure. Genotoxicity was assessed using the erythrocytes' micronucleus (MN) assay, while apoptosis was evaluated in nucleated blood cells. The results showed that Cr(III) (CrK(SO4)2 and CrCl3) did not induce any marked genotoxic damage. However, Cr(VI) (CrO3, K2Cr2O7, Na2Cr2O7, and K2CrO4) produced varying degrees of genotoxicity, with CrO3 being the most potent. MN frequencies increased following 24‐h exposure, with a greater effect in male mice. Administering 20 mg/kg of CrO3 via gavage did not lead to significant effects compared to intraperitoneal administration. Short‐term oral treatment with a daily dose of 8.5 mg/kg for 49 days elevated MN levels only on day 14 after treatment. Pregnant female mice exposed to CrO3 on day 15 of pregnancy exhibited reduced genotoxic effects compared to nonpregnant animals. However, significant increases in MN levels were found in their fetuses starting 48 h after exposure. In summary, data indicate the potential genotoxic effects of Cr, with Cr(VI) forms inducing higher genotoxicity than Cr(III). These findings indicate that gender, exposure route, and pregnancy status might influence genotoxic responses to Cr.

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Section: Apoptosis Necrosis and Cell Viabilitysupporting

confidence: 84%

Section: Apoptosis Necrosis and Cell Viabilitymentioning

confidence: 99%

A comparative study on chromium‐induced micronuclei assessment in the peripheral blood of Hsd:ICR mice

García‐Rodríguez,

Hernández‐Cortés,

Montaño‐Rodríguez

et al. 2023

J of Applied Toxicology

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“…A similar phenomenon has been found in green tea polyphenols, which could decrease oxidative DNA damage caused by exposure to metals. An in-depth study found that green tea polyphenols might directly eliminate free radicals, activate the repair oxidative DNA damage mechanism, or regulate the endogenous antioxidant system to decrease the DNA damage ( García-Rodríguez et al, 2023 ). Therefore, we deduced that the polyphenols from MPPAE could stimulate the activities of SOD and further protect against Cd-induced kidney injury.…”

Section: Discussionmentioning

confidence: 99%

Masson pine pollen aqueous extract ameliorates cadmium-induced kidney damage in rats

Hu,

Chen,

Shi

et al. 2023

Front. Mol. Biosci.

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Introduction: Cadmium (Cd) is a hazardous environmental pollutant present in soil, water, and food. Accumulation of Cd in organisms can cause systematic injury and damage to the kidney. The Masson pine pollen aqueous extract (MPPAE) has attracted increasing attention due to its antioxidant activity and ability to enhance immunity.Methods: In this study, we investigated the potential of MPPAE to protect against Cd-induced kidney damage in rats and the underlying mechanism. The transcriptome and metabolome of rats with Cd-induced kidney damage, following treatment with MPPAE, were explored.Results: The concentrations of superoxide dismutase (SOD) and malondialdehyde (MDA) were both significantly altered after treatment with MPPAE. Furthermore, sequencing and analysis of the transcriptome and metabolome of rats with Cd-induced kidney damage, following treatment with MPPAE, revealed differential expression of numerous genes and metabolites compared with the untreated control rats. These differentially expressed genes (DEGs) included detoxification-related genes such as cytochrome P450 and the transporter. The differentially expressed metabolites (DEMs) included 4-hydroxybenzoic acid, L-ascorbate, and ciliatine. Conjoint transcriptome and metabolome analysis showed that several DEGs were correlated with DEMs.Conclusion: These preliminary findings indicate the potential of MPPAE for the treatment of toxic metal poisoning.

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“…Each of these molecules and their iron or other metal complexes have diverse biological, pharmacological, and toxicological activity. In cancer, for example, the activity of such molecules may range from pro-oxidant and pro-carcinogenic to antioxidant and anti-carcinogenic effects and also many other effects, including the enhancement or inhibition of ferroptosis [ 187 , 188 , 189 , 190 , 191 , 192 , 193 , 194 ]. Similarly, many old and new carcinogens may contain or interact with iron, including food additives and coloring agents, many industrial and other chemicals, inhaled carcinogens from smoke, and other compounds from environmental pollution ( Table 1 ) [ 195 , 196 , 197 ].…”

Section: Iron Toxicity From Labile Forms Of Iron and Other Molecular ...mentioning

confidence: 99%

Iron Load Toxicity in Medicine: From Molecular and Cellular Aspects to Clinical Implications

Kontoghiorghes

2023

IJMS

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Iron is essential for all organisms and cells. Diseases of iron imbalance affect billions of patients, including those with iron overload and other forms of iron toxicity. Excess iron load is an adverse prognostic factor for all diseases and can cause serious organ damage and fatalities following chronic red blood cell transfusions in patients of many conditions, including hemoglobinopathies, myelodyspasia, and hematopoietic stem cell transplantation. Similar toxicity of excess body iron load but at a slower rate of disease progression is found in idiopathic haemochromatosis patients. Excess iron deposition in different regions of the brain with suspected toxicity has been identified by MRI T2* and similar methods in many neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease. Based on its role as the major biological catalyst of free radical reactions and the Fenton reaction, iron has also been implicated in all diseases associated with free radical pathology and tissue damage. Furthermore, the recent discovery of ferroptosis, which is a cell death program based on free radical generation by iron and cell membrane lipid oxidation, sparked thousands of investigations and the association of iron with cardiac, kidney, liver, and many other diseases, including cancer and infections. The toxicity implications of iron in a labile, non-protein bound form and its complexes with dietary molecules such as vitamin C and drugs such as doxorubicin and other xenobiotic molecules in relation to carcinogenesis and other forms of toxicity are also discussed. In each case and form of iron toxicity, the mechanistic insights, diagnostic criteria, and molecular interactions are essential for the design of new and effective therapeutic interventions and of future targeted therapeutic strategies. In particular, this approach has been successful for the treatment of most iron loading conditions and especially for the transition of thalassemia from a fatal to a chronic disease due to new therapeutic protocols resulting in the complete elimination of iron overload and of iron toxicity.

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Effects of green tea polyphenols against metal-induced genotoxic damage: underlying mechanistic pathways

Cited by 6 publications

References 91 publications

A comparative study on chromium‐induced micronuclei assessment in the peripheral blood of Hsd:ICR mice

A comparative study on chromium‐induced micronuclei assessment in the peripheral blood of Hsd:ICR mice

Masson pine pollen aqueous extract ameliorates cadmium-induced kidney damage in rats

Iron Load Toxicity in Medicine: From Molecular and Cellular Aspects to Clinical Implications

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