The aim of this study was to compare the effects of waterbome copper (Cu) and cadmium (Cd) on survival, anti-oxida- tive response, lipid peroxidation and metal accumulation in abalone Haliotis discus hannai. Exper...The aim of this study was to compare the effects of waterbome copper (Cu) and cadmium (Cd) on survival, anti-oxida- tive response, lipid peroxidation and metal accumulation in abalone Haliotis discus hannai. Experimental animals (initial weight: 7.49 g±0.01 g) were exposed to graded concentrations of waterborne Cu (0.02, 0.04, 0.06, 0.08 mg L-1) or Cd (0.025, 0.05, 0.25, 0.5 mgL-1) for 28 days, respectively. Activities of the anti-oxidative enzymes (catalase, CAT; superoxide dismutase, SOD; glutathione peroxidases, GPx; glutathione S-transferase, GST), contents of the reduced glutathione (GSH) and malondiadehyde (MDA) in the hepatopancreas, and metal accumulation in hepatopancreas and muscles were analyzed after 0, 1, 3, 6, 10, 15, 21, 28 days of metal exposure, respectively. Results showed that 0.04 mg L-1, 0.06 mg L-1 and 0.08 mgL-1 Cu caused 100% death of abalone on the 21st, 10th and 6th day, respectively. However, no dead abalone was found during the 28-day waterborne Cd exposure at all experimental concentrations. Generally, activities of SOD and GST in hepatopancreas under all Cu concentrations followed a decrease trend as the exposure time prolonged. However, these activities were firstly increased and then decreased to the control level and increased again during Cd exposure. Activities of CAT in all Cu exposure treatments were higher than those in the control. These activities were firstly increased and then decreased to the control level and increased again during Cd exposure. Contents of MDA in hepatopancreas in all Cu treatments significantly increased first and then decreased to the control level. However, the MDA contents in hepatopan- creas were not significantly changed during the 28-day Cd exposure. The metals accumulation in both hepatopancreas and muscles of abalone significantly increased with the increase of waterborne metals concentration and exposure time. These results indicated that H. discus hannai has a positive anti-oxidative defense against Cu or Cd. In conclusion, anti-oxidative mechanism in abalone to resist waterborne Cu did not follow the same pattern as that for waterborne Cd.展开更多
Aim To study the effect of Isorhapontigenin (Iso) on copper-mediatedperoxidation of human low-density lipoprotein (LDL) and on the toxicity of oxidized LDL (ox-LDL) tomouse macrophages in vitro. Methods Human LDL from...Aim To study the effect of Isorhapontigenin (Iso) on copper-mediatedperoxidation of human low-density lipoprotein (LDL) and on the toxicity of oxidized LDL (ox-LDL) tomouse macrophages in vitro. Methods Human LDL from sera df normal lipidemic donors was separated bysequential ultracentrifugation. The separated human IDL 1 mg·mL^(-1) in phosphate buffer saline, pH7.4, was incubated with cupric sulfate (10 μmol·L^(-1) ) at 37℃ for 10 h in the presence orabsence of various concentrations of Iso. Malondialdehyde (MDA) formation, vitamin E consumption,electrophoretic mobility of LDL, mitochondria] membrane potential of mouse peritoneal macrophages,phagocytosis of neutral red, and release of nitric oxide (NO) from macrophages were determined byvarious methods. Results Iso 1 - 100 μmol·L^(-1) significantly inhibited the increase of MDAformation, vitamin E consumption and electrophoretic mobility of LDL induced by Cu^(2+) in aconcentration-dependent manner. The injury of the mitochondrial membrane potential of mouseperitoneal macrophages due to incubation with ox-LDL (0.1 mg·mL^(-1)) at 37℃ for 12 h was markedlyprotected by 10 μmol·L^(-1) Iso. After pretreat-ment of the macrophages with 10 μmol · L^(-1)of Iso and then exposure to ox-LDL for 4 h, the reduction of phagocytosis of neutral red and releaseof NO in response to lipopolysaccharide (IPS) stimulation were significantly prevented. ConclusionIso has protective action against Cu^(2+) - mediated LDL peroxidation and ox-LDL induced toxicity tomacrophages in vitro.展开更多
Objective: To investigate serum level of SOD, MDA, ox-LDL, AchE and Ach in AD, to study atorvastatin influence on serum level of SOD, MDA, ox-LDL, Ache and Ach in AD and its neuroprotection mechanisms. Methods Subjec...Objective: To investigate serum level of SOD, MDA, ox-LDL, AchE and Ach in AD, to study atorvastatin influence on serum level of SOD, MDA, ox-LDL, Ache and Ach in AD and its neuroprotection mechanisms. Methods Subjects were divided into: normal blood lipid level group with Alzheimer's disease (A), higher blood lipid level group with Alzheimer's disease (AH), normal blood lipid level Alzheimer's disease group with atorvastatin treeatment (AT), higher blood lipid level Alzheimer's disease group with atorvastatin treeatment(AHT). Ox-LDL was measured by enzyme linked immunosorbent assay; SOD, MDA, ox-LDL, AchE, Ach and blood lipid level in AD was measured by biochemistry. Results: The serum level of MDA, Ache in AH group after atorvastatin treatment is lower ;The serum level of SOD, Ach in AH group is more increased than that of in A group; The serum level of ox-LDL in AH, A groups is lower than that of in A group; The dementia degree is lower after atorvastatin treatment. Conclusion: Atorvastatin can decrease serum level of MDA, AchE and ox-LDL, and increase that of SOD, Ach, and attenuate dementia symptom in AD, especially, with hyperlipemia. The hypothesis of atorvastatin neuroprotection is concluded that atorvastatin may restrain free radical reaction and retard oxidation in AD.展开更多
The objective of the present study was to determine the effect of different sources of dietary fibre on the oxidative stress induced by a high fat diet in laboratory rats. Thirty two laboratory rats were penned indivi...The objective of the present study was to determine the effect of different sources of dietary fibre on the oxidative stress induced by a high fat diet in laboratory rats. Thirty two laboratory rats were penned individually and divided into four groups: CONT (high fat diet), G (70 g guar gum/kg), P (70 g apple pectin/kg) and WB (155 g wheat bran/kg). After 11 or 13 days of treatment DNA damage of blood leukocytes was measured by Comet assay and lipid peroxidation was studied by determining the malondialdehyde (MDA) concentration in liver and in urine. In comparison with group CONT, the degree of DNA damage was significantly lower in group WB. In groups G and P DNA damage was also reduced but not significantly. Similar results were also obtained for the liver MDA concentration. All three studied groups showed reduced liver MDA concentrations but only group WB was significant compared to group CONT. In comparison with group CONT, the groups WB and P had significantly reduced 24-hour urine MDA excretion, hut not group G. The results of the experiment confirmed that wheat bran intake effectively reduces oxidative stress induced by a high fat diet.展开更多
Objective:The aim of this study was to investigate lipid disorders and lipid peroxidation associated with the malignant transformation of colorectal adenoma.Methods:Analyses were based on data from 100 subjects with h...Objective:The aim of this study was to investigate lipid disorders and lipid peroxidation associated with the malignant transformation of colorectal adenoma.Methods:Analyses were based on data from 100 subjects with histologically confirmed adenomas(cases) and 50 adenoma-free control subjects,all of whom had colonoscopy.The subjects were divided into two groups:those with no adenoma and those with adenoma.According to subsite of adenomas the subjects with adenoma were divided into group of distal adenoma and group of proximal adenoma.According to histology of adenomas the subjects with adenoma were divided into group of villiform adenoma and group of tubular + tubulo-villous adenoma.Among the groups,the serum levels of triglyceride(TG),total cholesterol(TC),high density lipoprotein cholesterol(HDL-C),lowdensity lipoprotein cholesterol(LDL-C),and lipid peroxidation product malondialdehyde(MDA) were compared in all the patients.Results:Plasma total cholesterol and MDA level in group of adenomas were significantly higher than that in group of control subjects,but plasma HDL-C level was low in group of adenomas(P<0.05).Plasma total cholesterol and MDA levels were positively related to distal and villiform adenomas(P<0.05).Conclusion:The findings suggest that altered lipid metabolism may be differentially associated with colorectal adenomas.展开更多
基金financially supported by grant from the National Natural Science Foundation of China (No. 30972262)
文摘The aim of this study was to compare the effects of waterbome copper (Cu) and cadmium (Cd) on survival, anti-oxida- tive response, lipid peroxidation and metal accumulation in abalone Haliotis discus hannai. Experimental animals (initial weight: 7.49 g±0.01 g) were exposed to graded concentrations of waterborne Cu (0.02, 0.04, 0.06, 0.08 mg L-1) or Cd (0.025, 0.05, 0.25, 0.5 mgL-1) for 28 days, respectively. Activities of the anti-oxidative enzymes (catalase, CAT; superoxide dismutase, SOD; glutathione peroxidases, GPx; glutathione S-transferase, GST), contents of the reduced glutathione (GSH) and malondiadehyde (MDA) in the hepatopancreas, and metal accumulation in hepatopancreas and muscles were analyzed after 0, 1, 3, 6, 10, 15, 21, 28 days of metal exposure, respectively. Results showed that 0.04 mg L-1, 0.06 mg L-1 and 0.08 mgL-1 Cu caused 100% death of abalone on the 21st, 10th and 6th day, respectively. However, no dead abalone was found during the 28-day waterborne Cd exposure at all experimental concentrations. Generally, activities of SOD and GST in hepatopancreas under all Cu concentrations followed a decrease trend as the exposure time prolonged. However, these activities were firstly increased and then decreased to the control level and increased again during Cd exposure. Activities of CAT in all Cu exposure treatments were higher than those in the control. These activities were firstly increased and then decreased to the control level and increased again during Cd exposure. Contents of MDA in hepatopancreas in all Cu treatments significantly increased first and then decreased to the control level. However, the MDA contents in hepatopan- creas were not significantly changed during the 28-day Cd exposure. The metals accumulation in both hepatopancreas and muscles of abalone significantly increased with the increase of waterborne metals concentration and exposure time. These results indicated that H. discus hannai has a positive anti-oxidative defense against Cu or Cd. In conclusion, anti-oxidative mechanism in abalone to resist waterborne Cu did not follow the same pattern as that for waterborne Cd.
文摘Aim To study the effect of Isorhapontigenin (Iso) on copper-mediatedperoxidation of human low-density lipoprotein (LDL) and on the toxicity of oxidized LDL (ox-LDL) tomouse macrophages in vitro. Methods Human LDL from sera df normal lipidemic donors was separated bysequential ultracentrifugation. The separated human IDL 1 mg·mL^(-1) in phosphate buffer saline, pH7.4, was incubated with cupric sulfate (10 μmol·L^(-1) ) at 37℃ for 10 h in the presence orabsence of various concentrations of Iso. Malondialdehyde (MDA) formation, vitamin E consumption,electrophoretic mobility of LDL, mitochondria] membrane potential of mouse peritoneal macrophages,phagocytosis of neutral red, and release of nitric oxide (NO) from macrophages were determined byvarious methods. Results Iso 1 - 100 μmol·L^(-1) significantly inhibited the increase of MDAformation, vitamin E consumption and electrophoretic mobility of LDL induced by Cu^(2+) in aconcentration-dependent manner. The injury of the mitochondrial membrane potential of mouseperitoneal macrophages due to incubation with ox-LDL (0.1 mg·mL^(-1)) at 37℃ for 12 h was markedlyprotected by 10 μmol·L^(-1) Iso. After pretreat-ment of the macrophages with 10 μmol · L^(-1)of Iso and then exposure to ox-LDL for 4 h, the reduction of phagocytosis of neutral red and releaseof NO in response to lipopolysaccharide (IPS) stimulation were significantly prevented. ConclusionIso has protective action against Cu^(2+) - mediated LDL peroxidation and ox-LDL induced toxicity tomacrophages in vitro.
基金Supported by the Doctoral Project of Chongqing Medical University(2006010068).
文摘Objective: To investigate serum level of SOD, MDA, ox-LDL, AchE and Ach in AD, to study atorvastatin influence on serum level of SOD, MDA, ox-LDL, Ache and Ach in AD and its neuroprotection mechanisms. Methods Subjects were divided into: normal blood lipid level group with Alzheimer's disease (A), higher blood lipid level group with Alzheimer's disease (AH), normal blood lipid level Alzheimer's disease group with atorvastatin treeatment (AT), higher blood lipid level Alzheimer's disease group with atorvastatin treeatment(AHT). Ox-LDL was measured by enzyme linked immunosorbent assay; SOD, MDA, ox-LDL, AchE, Ach and blood lipid level in AD was measured by biochemistry. Results: The serum level of MDA, Ache in AH group after atorvastatin treatment is lower ;The serum level of SOD, Ach in AH group is more increased than that of in A group; The serum level of ox-LDL in AH, A groups is lower than that of in A group; The dementia degree is lower after atorvastatin treatment. Conclusion: Atorvastatin can decrease serum level of MDA, AchE and ox-LDL, and increase that of SOD, Ach, and attenuate dementia symptom in AD, especially, with hyperlipemia. The hypothesis of atorvastatin neuroprotection is concluded that atorvastatin may restrain free radical reaction and retard oxidation in AD.
文摘The objective of the present study was to determine the effect of different sources of dietary fibre on the oxidative stress induced by a high fat diet in laboratory rats. Thirty two laboratory rats were penned individually and divided into four groups: CONT (high fat diet), G (70 g guar gum/kg), P (70 g apple pectin/kg) and WB (155 g wheat bran/kg). After 11 or 13 days of treatment DNA damage of blood leukocytes was measured by Comet assay and lipid peroxidation was studied by determining the malondialdehyde (MDA) concentration in liver and in urine. In comparison with group CONT, the degree of DNA damage was significantly lower in group WB. In groups G and P DNA damage was also reduced but not significantly. Similar results were also obtained for the liver MDA concentration. All three studied groups showed reduced liver MDA concentrations but only group WB was significant compared to group CONT. In comparison with group CONT, the groups WB and P had significantly reduced 24-hour urine MDA excretion, hut not group G. The results of the experiment confirmed that wheat bran intake effectively reduces oxidative stress induced by a high fat diet.
基金Supported in part by Natural Science Foundation of Hubei Province (No. 302-131703)
文摘Objective:The aim of this study was to investigate lipid disorders and lipid peroxidation associated with the malignant transformation of colorectal adenoma.Methods:Analyses were based on data from 100 subjects with histologically confirmed adenomas(cases) and 50 adenoma-free control subjects,all of whom had colonoscopy.The subjects were divided into two groups:those with no adenoma and those with adenoma.According to subsite of adenomas the subjects with adenoma were divided into group of distal adenoma and group of proximal adenoma.According to histology of adenomas the subjects with adenoma were divided into group of villiform adenoma and group of tubular + tubulo-villous adenoma.Among the groups,the serum levels of triglyceride(TG),total cholesterol(TC),high density lipoprotein cholesterol(HDL-C),lowdensity lipoprotein cholesterol(LDL-C),and lipid peroxidation product malondialdehyde(MDA) were compared in all the patients.Results:Plasma total cholesterol and MDA level in group of adenomas were significantly higher than that in group of control subjects,but plasma HDL-C level was low in group of adenomas(P<0.05).Plasma total cholesterol and MDA levels were positively related to distal and villiform adenomas(P<0.05).Conclusion:The findings suggest that altered lipid metabolism may be differentially associated with colorectal adenomas.