Objective To investigate the effects of fluoride on lipid peroxidation, DNA damage and apoptosis in human embryo hepatocyte L-02 cells. Methods Lipid peroxide (LPO) level, reduced glutathione (GSH) content, DNA damage...Objective To investigate the effects of fluoride on lipid peroxidation, DNA damage and apoptosis in human embryo hepatocyte L-02 cells. Methods Lipid peroxide (LPO) level, reduced glutathione (GSH) content, DNA damage, apoptosis, and cell cycle analysis were measured after in vitro cultured L-02 cells were exposed to sodium fluoride at different doses (40 μg/mL, 80 μg/mL, and 160 μg/mL) for 24 hours. Results Fluoride caused an increase of LPO levels and a decrease of GSH content in L-02 cells. There appeared to be an obvious dose-effect relationship between the fluoride concentration and the observed changes. Fluoride also caused DNA damage and apoptosis and increased the cell number in S phase of cell cycle in the cells tested. There was a statistically significant difference in DNA damage and apoptosis when comparing the high dose of fluoride treated cells with the low dose of fluoride treated cells. Conclusion Fluoride can cause lipid peroxidation, DNA damage, and apoptosis in the L-02 cell experimental model and there is a significant positive correlation between fluoride concentration and these pathological changes.展开更多
Objective To evaluate the oxidative stress in patients with colorectal cancer and to investigate the relationship between oxidative stress and colorectal cancer. Methods Seventy-six subjects were divided into two grou...Objective To evaluate the oxidative stress in patients with colorectal cancer and to investigate the relationship between oxidative stress and colorectal cancer. Methods Seventy-six subjects were divided into two groups （36 colorectal cancer patients as the study group and 40 normal healthy individuals as the control group）. Their protein oxidation, DNA damage, lipid peroxidation and antioxidants, vitamin C, vitamin E, glutathione （GSH）, and antioxidative enzymes in serum were detected. Results The levels of protein carbonyl and advanced oxidation protein products （AOPP） were significantly higher in the study group than in the control group （P〈0.01）. Serum 8-OHdG was significantly increased in the study group compared to the control group （P〈0.01）. However, the mean serum level of MDA and conjugated diene was lower in the study group than in the control group （P〈0.01）. The activity of antioxidative enzymes was significantly decreased in the study group compared to the control group （P〈0.01）. Serum vitamins C and E concentrations were significantly reduced in the study group compared to the control group （P〈0.01）. Conclusion Colorectal cancer is associated with oxidative stress, and assessment of oxidative stress and given antioxidants is important for the treatment and prevention of colorectal cancer.展开更多
Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enro...Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enrolled in a casecontrol study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers （HAV）, on whom plasma nitric oxide （NO）, vitamin C （VC）, vitamin E （VE） and β-carotene （β-CAR） level, erythrocyte malondialdehyde （MDA） level, as well as erythrocyte superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX） activities were determined by spectrophotometry. Results： Compared with the HAV group, values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased （P 〈 0.001）; those of plasma VC, VE and β-CAR as well as erythrocyte SOD, CAT and GPX activities in the CBPP group were significantly decreased （P 〈 0.001）. Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease, values of NO and MDA were gradually increased （P 〈 0.001）, and those of VC, VE, β-CAR, SOD, CAT and GPX were gradually decreased （P 〈 0.05- 0.001）. The findings from stepwise regression for the 70 CBPP suggested that the model was Y= -13.2077 ＋ 0.1894MDA ＋ 0.0415NO - 0.1999GPX, F = 18.2047, P 〈 0.001, r = 0.6729, P 〈 0.001. Conclusion： The findings suggest that there exist increased oxidative stress and oxidative damage induced by chronic bacterial prostatitis in the patients, and such phenomenon was closely related to the course of disease.展开更多
Myocardial ischemia/reperfusion(/R)injury is a classic type of cardiovascular disease characterized by injury to cardiomyocytes leading to various forms of cell death.It is believed that irreversible myocardial damage...Myocardial ischemia/reperfusion(/R)injury is a classic type of cardiovascular disease characterized by injury to cardiomyocytes leading to various forms of cell death.It is believed that irreversible myocardial damage resulted from I/R occurs due to oxidative stress evoked during the reperfusion phase.Here we demonstrate that ischemia triggers a specific redox reaction of polyunsaturated fatty acids(PUFA)-phospholipids in myocardial cells,which acts as a priming signaling that initiates the outbreak of robust oxidative damage in the reperfusion phase.Using animal and in vitro models,the crucial lipid species in I/R injury were identifed to be oxidized PUFAs enriched phosphatidylethanolamines.Using multi-omics,arachidonic acid 15-lipoxygenase-1(ALOx15)was identified as the primary mediator of ischemia-provoked phospholipid peroxidation,which was further confirmed using chemogenetic approaches.Collectively,our results reveal that ALOx15 induction in the ischemia phase acts as a"burning point"to ignite phospholipid oxidization into ferroptotic signals.This finding characterizes a novel molecular mechanism for myocardial ischemia injury and offers a potential therapeutic target for early intervention of V/R injury.展开更多
基金The work was supported by grants from the National Nature Science Foundation of China (No. 30271155) China national key basic research and development program (No. 2022CB512908).
文摘Objective To investigate the effects of fluoride on lipid peroxidation, DNA damage and apoptosis in human embryo hepatocyte L-02 cells. Methods Lipid peroxide (LPO) level, reduced glutathione (GSH) content, DNA damage, apoptosis, and cell cycle analysis were measured after in vitro cultured L-02 cells were exposed to sodium fluoride at different doses (40 μg/mL, 80 μg/mL, and 160 μg/mL) for 24 hours. Results Fluoride caused an increase of LPO levels and a decrease of GSH content in L-02 cells. There appeared to be an obvious dose-effect relationship between the fluoride concentration and the observed changes. Fluoride also caused DNA damage and apoptosis and increased the cell number in S phase of cell cycle in the cells tested. There was a statistically significant difference in DNA damage and apoptosis when comparing the high dose of fluoride treated cells with the low dose of fluoride treated cells. Conclusion Fluoride can cause lipid peroxidation, DNA damage, and apoptosis in the L-02 cell experimental model and there is a significant positive correlation between fluoride concentration and these pathological changes.
基金the grant from the Health Bureau of Heilongjiang Province (No. 2005-126)the Natural Science Foundation of Heilongjiang Province (No. D2007-29)
文摘Objective To evaluate the oxidative stress in patients with colorectal cancer and to investigate the relationship between oxidative stress and colorectal cancer. Methods Seventy-six subjects were divided into two groups （36 colorectal cancer patients as the study group and 40 normal healthy individuals as the control group）. Their protein oxidation, DNA damage, lipid peroxidation and antioxidants, vitamin C, vitamin E, glutathione （GSH）, and antioxidative enzymes in serum were detected. Results The levels of protein carbonyl and advanced oxidation protein products （AOPP） were significantly higher in the study group than in the control group （P〈0.01）. Serum 8-OHdG was significantly increased in the study group compared to the control group （P〈0.01）. However, the mean serum level of MDA and conjugated diene was lower in the study group than in the control group （P〈0.01）. The activity of antioxidative enzymes was significantly decreased in the study group compared to the control group （P〈0.01）. Serum vitamins C and E concentrations were significantly reduced in the study group compared to the control group （P〈0.01）. Conclusion Colorectal cancer is associated with oxidative stress, and assessment of oxidative stress and given antioxidants is important for the treatment and prevention of colorectal cancer.
文摘Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enrolled in a casecontrol study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers （HAV）, on whom plasma nitric oxide （NO）, vitamin C （VC）, vitamin E （VE） and β-carotene （β-CAR） level, erythrocyte malondialdehyde （MDA） level, as well as erythrocyte superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX） activities were determined by spectrophotometry. Results： Compared with the HAV group, values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased （P 〈 0.001）; those of plasma VC, VE and β-CAR as well as erythrocyte SOD, CAT and GPX activities in the CBPP group were significantly decreased （P 〈 0.001）. Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease, values of NO and MDA were gradually increased （P 〈 0.001）, and those of VC, VE, β-CAR, SOD, CAT and GPX were gradually decreased （P 〈 0.05- 0.001）. The findings from stepwise regression for the 70 CBPP suggested that the model was Y= -13.2077 ＋ 0.1894MDA ＋ 0.0415NO - 0.1999GPX, F = 18.2047, P 〈 0.001, r = 0.6729, P 〈 0.001. Conclusion： The findings suggest that there exist increased oxidative stress and oxidative damage induced by chronic bacterial prostatitis in the patients, and such phenomenon was closely related to the course of disease.
基金This work was supported,in part,by National Key Research and Development Program of China(2017YFC1700400,2017YFC1700404,2022YFC0867400)Natural Science Foundation of China(82125038,81904068,81873209,U1801284,81903821,82174054)+3 种基金the Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program(2017BT01 Y036)GDUPS(2019),Natural Science Foundation of Guangdong(2019A1515010909,2021A1515011297)Science and Technology Program of Guangzhou(201903010062,907158833068)the Innovation Team Project of Guangdong Provincial Department of Education(2020KCXTD003).
文摘Myocardial ischemia/reperfusion(/R)injury is a classic type of cardiovascular disease characterized by injury to cardiomyocytes leading to various forms of cell death.It is believed that irreversible myocardial damage resulted from I/R occurs due to oxidative stress evoked during the reperfusion phase.Here we demonstrate that ischemia triggers a specific redox reaction of polyunsaturated fatty acids(PUFA)-phospholipids in myocardial cells,which acts as a priming signaling that initiates the outbreak of robust oxidative damage in the reperfusion phase.Using animal and in vitro models,the crucial lipid species in I/R injury were identifed to be oxidized PUFAs enriched phosphatidylethanolamines.Using multi-omics,arachidonic acid 15-lipoxygenase-1(ALOx15)was identified as the primary mediator of ischemia-provoked phospholipid peroxidation,which was further confirmed using chemogenetic approaches.Collectively,our results reveal that ALOx15 induction in the ischemia phase acts as a"burning point"to ignite phospholipid oxidization into ferroptotic signals.This finding characterizes a novel molecular mechanism for myocardial ischemia injury and offers a potential therapeutic target for early intervention of V/R injury.
