Coenzyme Q10 protects isolated human blood cells from TiO<inf>2</inf> nanoparticles induced oxidative/antioxidative imbalance, hemolysis, cytotoxicity, DNA damage and mitochondrial impairment
Authors: Wani, M.R. and Shadab, G.G.H.A.
Journal: Molecular Biology Reports
Volume: 48
Issue: 4
Pages: 3367-3377
eISSN: 1573-4978
ISSN: 0301-4851
DOI: 10.1007/s11033-021-06394-x
Abstract:TiO2 NPs have been investigated for their toxic potential and studies have reported their toxicity is due to generation of oxidative stress. In the present study, we investigated the toxicity of TiO2 NPs and explored the potential of well-known antioxidant coenzyme Q10 (CoQ10) in counteracting the NP-induced toxicity in isolated human blood cells. When the isolated blood cells were treated with varying concentrations of TiO2 NPs (25–100 μg/ml), only 50 μg/ml dose induced statistically significant hemolysis in erythrocytes and cytotoxicity in lymphocytes (p < 0.05). None of the concentrations induced any significant increase in platelet aggregation. To investigate the protective effect of CoQ10, we incubated the isolated blood cells with 50 μg/ml of TiO2 NPs in the presence and absence of 25 μM of CoQ10 for 3 h. Hemolysis, oxidative stress, LDH leakage and ATPase enzyme activity were studied in erythrocytes; cytotoxic and DNA damaging potential of NPs were determined in lymphocytes, along with mitochondrial membrane potential (MMP) and ADP/ATP ratio. Hemolysis, generation of oxidative stress, LDH leakage and reduced ATPase activity were observed in the erythrocytes treated with NPs alone (50 μg/ml), the results were statistically significant at p < 0.05. Oxidative stress was evident by increased levels of malonaldehyde, indicating lipid peroxidation and generation of reactive oxygen species including hydrogen peroxide, together with statistically significant decrease in the activities of catalase and superoxide dismutase and reduced glutathione levels. In the lymphocytes treated with NPs alone (50 μg/ml), cytotoxicity in MTT assay and DNA damage in comet assay were observed; in addition, mitochondrial membrane potential collapsed and ADP/ATP ratio increased indicating mitochondrial function impairment. However, in the presence of CoQ10, hemolysis, oxidative stress and LDH leakage in the erythrocytes and lymphocyte cytotoxicity and DNA damage were drastically reduced, enzyme activities, MMP and ADP/ATP ratio were restored towards normal levels. TiO2 NPs induce cytotoxicity, damage DNA in lymphocytes, and induce oxidative/anti-oxidative imbalance in erythrocytes. Antioxidant CoQ10 protects erythrocytes and lymphocytes from toxicity induced by TiO2 NPs.
Source: Scopus
Coenzyme Q10 protects isolated human blood cells from TiO2 nanoparticles induced oxidative/antioxidative imbalance, hemolysis, cytotoxicity, DNA damage and mitochondrial impairment.
Authors: Wani, M.R. and Shadab, G.G.H.A.
Journal: Mol Biol Rep
Volume: 48
Issue: 4
Pages: 3367-3377
eISSN: 1573-4978
DOI: 10.1007/s11033-021-06394-x
Abstract:TiO2 NPs have been investigated for their toxic potential and studies have reported their toxicity is due to generation of oxidative stress. In the present study, we investigated the toxicity of TiO2 NPs and explored the potential of well-known antioxidant coenzyme Q10 (CoQ10) in counteracting the NP-induced toxicity in isolated human blood cells. When the isolated blood cells were treated with varying concentrations of TiO2 NPs (25-100 μg/ml), only 50 μg/ml dose induced statistically significant hemolysis in erythrocytes and cytotoxicity in lymphocytes (p < 0.05). None of the concentrations induced any significant increase in platelet aggregation. To investigate the protective effect of CoQ10, we incubated the isolated blood cells with 50 μg/ml of TiO2 NPs in the presence and absence of 25 μM of CoQ10 for 3 h. Hemolysis, oxidative stress, LDH leakage and ATPase enzyme activity were studied in erythrocytes; cytotoxic and DNA damaging potential of NPs were determined in lymphocytes, along with mitochondrial membrane potential (MMP) and ADP/ATP ratio. Hemolysis, generation of oxidative stress, LDH leakage and reduced ATPase activity were observed in the erythrocytes treated with NPs alone (50 μg/ml), the results were statistically significant at p < 0.05. Oxidative stress was evident by increased levels of malonaldehyde, indicating lipid peroxidation and generation of reactive oxygen species including hydrogen peroxide, together with statistically significant decrease in the activities of catalase and superoxide dismutase and reduced glutathione levels. In the lymphocytes treated with NPs alone (50 μg/ml), cytotoxicity in MTT assay and DNA damage in comet assay were observed; in addition, mitochondrial membrane potential collapsed and ADP/ATP ratio increased indicating mitochondrial function impairment. However, in the presence of CoQ10, hemolysis, oxidative stress and LDH leakage in the erythrocytes and lymphocyte cytotoxicity and DNA damage were drastically reduced, enzyme activities, MMP and ADP/ATP ratio were restored towards normal levels. TiO2 NPs induce cytotoxicity, damage DNA in lymphocytes, and induce oxidative/anti-oxidative imbalance in erythrocytes. Antioxidant CoQ10 protects erythrocytes and lymphocytes from toxicity induced by TiO2 NPs.
Source: PubMed
Coenzyme Q10 protects isolated human blood cells from TiO<sub>2</sub> nanoparticles induced oxidative/antioxidative imbalance, hemolysis, cytotoxicity, DNA damage and mitochondrial impairment.
Authors: Wani, M.R. and Shadab, G.G.H.A.
Journal: Molecular biology reports
Volume: 48
Issue: 4
Pages: 3367-3377
eISSN: 1573-4978
ISSN: 0301-4851
DOI: 10.1007/s11033-021-06394-x
Abstract:TiO2 NPs have been investigated for their toxic potential and studies have reported their toxicity is due to generation of oxidative stress. In the present study, we investigated the toxicity of TiO2 NPs and explored the potential of well-known antioxidant coenzyme Q10 (CoQ10) in counteracting the NP-induced toxicity in isolated human blood cells. When the isolated blood cells were treated with varying concentrations of TiO2 NPs (25-100 μg/ml), only 50 μg/ml dose induced statistically significant hemolysis in erythrocytes and cytotoxicity in lymphocytes (p < 0.05). None of the concentrations induced any significant increase in platelet aggregation. To investigate the protective effect of CoQ10, we incubated the isolated blood cells with 50 μg/ml of TiO2 NPs in the presence and absence of 25 μM of CoQ10 for 3 h. Hemolysis, oxidative stress, LDH leakage and ATPase enzyme activity were studied in erythrocytes; cytotoxic and DNA damaging potential of NPs were determined in lymphocytes, along with mitochondrial membrane potential (MMP) and ADP/ATP ratio. Hemolysis, generation of oxidative stress, LDH leakage and reduced ATPase activity were observed in the erythrocytes treated with NPs alone (50 μg/ml), the results were statistically significant at p < 0.05. Oxidative stress was evident by increased levels of malonaldehyde, indicating lipid peroxidation and generation of reactive oxygen species including hydrogen peroxide, together with statistically significant decrease in the activities of catalase and superoxide dismutase and reduced glutathione levels. In the lymphocytes treated with NPs alone (50 μg/ml), cytotoxicity in MTT assay and DNA damage in comet assay were observed; in addition, mitochondrial membrane potential collapsed and ADP/ATP ratio increased indicating mitochondrial function impairment. However, in the presence of CoQ10, hemolysis, oxidative stress and LDH leakage in the erythrocytes and lymphocyte cytotoxicity and DNA damage were drastically reduced, enzyme activities, MMP and ADP/ATP ratio were restored towards normal levels. TiO2 NPs induce cytotoxicity, damage DNA in lymphocytes, and induce oxidative/anti-oxidative imbalance in erythrocytes. Antioxidant CoQ10 protects erythrocytes and lymphocytes from toxicity induced by TiO2 NPs.
Source: Europe PubMed Central