目的研究程序性细胞死亡蛋白4(programmed cell death protein 4,PDCD4)在脓毒症诱导的急性肾损伤(acute kidney injury,AKI)中的作用机制,以及调控PDCD4表达通过丝裂原活化蛋白激酶3(mitogen-activated protein kinase 3,MAP2K3)和p38...目的研究程序性细胞死亡蛋白4(programmed cell death protein 4,PDCD4)在脓毒症诱导的急性肾损伤(acute kidney injury,AKI)中的作用机制,以及调控PDCD4表达通过丝裂原活化蛋白激酶3(mitogen-activated protein kinase 3,MAP2K3)和p38蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)对脓毒症AKI起到潜在治疗作用。方法用脂多糖(lipopolysaccharide,LPS)刺激人肾小管上皮细胞(HK-2)构建脓毒症AKI细胞模型。进一步用腺病毒介导siRNA和过表达载体抑制和上调AKI细胞模型中PDCD4的表达;CCK-8法检测细胞增殖;用DCFH-DA及激光共聚焦显微镜检测细胞中ROS水平,用总SOD活性检测试剂和MDA检测试剂盒检测细胞中SOD和MDA水平;免疫共沉淀验证PDCD4和MAP2K3之间的蛋白相互作用;TUNEL染色法检测细胞凋亡;RT-qPCR和Western blot检测PDCD4及相关基因的mRNA和蛋白表达水平;ELISA法检测患者血清中炎症相关因子水平。结果LPS诱导可以促进HK-2细胞中PDCD4表达,下调PDCD4可抑制LPS诱导的HK-2细胞的炎症、氧化应激及细胞凋亡。数据库预测及免疫共沉淀证实PDCD4可以与MAP2K3相互作用,且在LPS诱导的HK-2细胞中,MAP2K3表达水平显著增强。MAP2K3过表达和p38 MAPK激动剂可以减轻PDCD4下调对LPS诱导的细胞炎症和氧化应激的影响并抑制细胞凋亡。结论下调PDCD4可以通过抑制MAP2K3和p38 MAPK从而抑制LPS诱导的肾小管上皮细胞的炎症和凋亡。展开更多
Although mutations in the superoxide dismutase 1 gene account for only a minority of total amyotrophic lateral sclerosis cases,the discovery of this gene has been crucial for amyotrophic lateral sclerosis research.Sin...Although mutations in the superoxide dismutase 1 gene account for only a minority of total amyotrophic lateral sclerosis cases,the discovery of this gene has been crucial for amyotrophic lateral sclerosis research.Since the identification of superoxide dismutase 1 in 1993,the field of amyotrophic lateral sclerosis genetics has considerably widened,improving our understanding of the diverse pathogenic basis of amyotrophic lateral sclerosis.In this review,we focus on cognitive impairment in superoxide dismutase 1-amyotrophic lateral sclerosis patients.Literature has mostly reported that cognition remains intact in superoxide dismutase 1-amyotrophic lateral sclerosis patients,but recent reports highlight frontal lobe function frailty in patients carrying different superoxide dismutase 1-amyotrophic lateral sclerosis mutations.We thoroughly reviewed all the various mutations reported in the literature to contribute to a comprehensive database of superoxide dismutase 1-amyotrophic lateral sclerosis genotype-phenotype correlation.Such a resource could ultimately improve our mechanistic understanding of amyotrophic lateral sclerosis,enabling a more robust assessment of how the amyotrophic lateral sclerosis phenotype responds to different variants across genes,which is important for the therapeutic strategy targeting genetic mutations.Cognition in superoxide dismutase 1-amyotrophic lateral sclerosis deserves further longitudinal research since this peculiar frailty in patients with similar mutations can be conditioned by external factors,including environment and other unidentified agents including modifier genes.展开更多
Amyotrophic lateral sclerosis is a very disabling disease due to the degeneration of motor neurons.Symptoms include muscle weakness and atrophy,spasticity,and progressive paralysis.Currently,there is no treatment to r...Amyotrophic lateral sclerosis is a very disabling disease due to the degeneration of motor neurons.Symptoms include muscle weakness and atrophy,spasticity,and progressive paralysis.Currently,there is no treatment to reverse damage to motor neurons and cure amyotrophic lateral sclerosis.The only two treatments actually approved,riluzole and edaravone,have shown mitigated beneficial effects.The difficulty to find a cure lies in the complexity and multifaceted pattern of amyotrophic lateral sclerosis pathogenesis.Among mechanisms,abnormal RNA metabolism,nucleocytoplasmic transport defects,accumulation of unfolded protein,and mitochondrial dysfunction would in fine induce oxidative damage and vice versa.A potent therapeutic strategy will be to find molecules that break this vicious circle.Sharpening the nuclear factor erythroid-2 related factor 2 signaling may fulfill this objective since nuclear factor erythroid-2 related factor 2 has a multitarget profile controlling antioxidant defense,mitochondrial functioning,and inflammation.We here discuss the interest of developing nuclear factor erythroid-2 related factor 2-based therapy in regard to the pathophysiological mechanisms and we provide a general overview of the attempted clinical assays in amyotrophic lateral sclerosis.展开更多
Objective To investigate the correlation between drinking behavior combined with polymorphisms of extracellular superoxide dismutase(EC-SOD) and aldehyde dehydrogenase-2(ALDH2) genes and pancreatic cancer. Methods The...Objective To investigate the correlation between drinking behavior combined with polymorphisms of extracellular superoxide dismutase(EC-SOD) and aldehyde dehydrogenase-2(ALDH2) genes and pancreatic cancer. Methods The genetic polymorphisms of EC-SOD and ALDH2 were analyzed by polymerase chain reaction restriction fragment length polymorphism in the peripheral blood leukocytes obtained from 680 pancreatic cancer cases and 680 non-cancer controls. Subsequently the frequency of genotype was compared between the pancreatic cancer patients and the healthy controls.The relationship of drinking with pancreatic cancer was analyzed. Results The frequencies of EC-SOD(C/G) and ALDH2 variant genotypes were 37.35% and 68.82% respectively in the pancreatic cancer cases, and were significantly higher than those in the healthy controls(21.03% and 44.56%, all P<0.01). People who carried EC-SOD(C/G)(OR=2.24, 95% CI= 1.81-4.03, P<0.01) or ALDH2 variant genotypes(OR=2.75, 95% CI=1.92-4.47, P<0.01) had a high risk to develop pancreatic cancer. Those who carried EC-SOD(C/G) genotype combined with ALDH2 variant genotype had a high risk for pancreatic cancer(29.56% vs. 6.76%, OR=7.69, 95% CI=3.58-10.51, P<0.01). The drinking rate of the pancreatic cancer group(64.12%) was significantly higher than that of the control group(40.15%; OR=2.66, 95% CI=1.30-4.42, P<0.01). An interaction between drinking and EC-SOD(C/G)/ALDH2 variant genotypes increased the risk of occurrence of pancreatic cancer(OR=25.00, 95% CI= 11.87-35.64, P<0.01). Conclusion EC-SOD(C/G), ALDH2 variant genotypes and drinking might be the risk factors of pancreatic cancer.展开更多
[Objective]This study was to investigate the effect of different concentrations of Norfloxacin on the superoxide dismutase ( SOD) activities in the blood plasma and liver tissues of Amur sturgeon ( Acipenser schrencki...[Objective]This study was to investigate the effect of different concentrations of Norfloxacin on the superoxide dismutase ( SOD) activities in the blood plasma and liver tissues of Amur sturgeon ( Acipenser schrencki Brandt) and sterlet ( Acipenser ruthenus Linnaeus) . [Method] Using pharmaco-toxicological evaluation method,Norfloxacin with the concentrations of 0,20,40,60,80 and 100 mg /kg,was orally delivered to the Amur sturgeon and sterlet for 5 d,respectively. The SOD activities in the blood plasma and liver tissues were measured after drug withdrawal for 2 d to explore the optimal dosing concentration of Norfloxacin during sturgeon culture,as well as the effect of Norfloxacin on liver injury. [Result] SOD existed in both two sturgeons but with different amounts,and the SOD activities were higher in the livers than in the blood plasma no matter in the control and all drug delivered groups. Under different drug delivery concentrations,the SOD activities first increased and then decreased in the 2 tissues of the 2 sturgeon species,and the SOD activities reached the maximum when the drug delivery concentration was 40 mg /kg. The drug de- livery concentration had little effect on the SOD activities in the blood plasma,which showed stable changes. When the drug delivery concentration was 40 mg /kg,the SOD activities in the blood plasma of Amur sturgeon were higher than that of sterlet,while for the other concentrations,the SOD activities in the plasma of sterlet showed higher performance. However,the SOD activities changed significantly through drug delivery in the liver tis- sues,and the SOD activities were higher in the sterlet than in the Amur sturgeon when the drug delivery concentrations were 0,40 and 100 mg /kg. The SOD activity in the sterlet was the highest under 40 mg /kg,presenting a sharp peak value. The optimal drug delivery concentration of Norfloxa- cin was 30 -50 mg /kg,under which the Norfloxacin presented best effect and had no injury effect on livers. [Conclusion]This study provides theo- retical basis for the reasonable application of Norfloxacin in aquaculture.展开更多
Superoxide dismutase (SOD) and ascorbate peroxidase (APX) play central roles in the pathway for scavenging reactive oxygen species in plants, thereby contributing to the tolerance against abiotic stress. Here we repor...Superoxide dismutase (SOD) and ascorbate peroxidase (APX) play central roles in the pathway for scavenging reactive oxygen species in plants, thereby contributing to the tolerance against abiotic stress. Here we report the responses of cytosolic SOD (cSOD; sodCc1 and sodCc2) and cytosolic APX (cAPX; OsAPX1 and OsAPX2) genes to oxidative and abiotic stress in rice. RNA blot analyses revealed that methyl viologen treatment caused a more prominent induction of cAPXs compared with cSODs, and hydrogen peroxide treatment induced the expression of cAPXs whereas cSODs were not affected. These results suggest that cAPXs play more important roles in defense against oxidative stress compared with cSODs. It is noted that cSODs and cAPXs showed coordinate response to abscisic acid treatment which induced both sodCc1 and OsAPX2. However, cSODs and cAPXs responded differentially to drought, salt and chilling stress, which indicates that cSOD and cAPX genes are expressed differentially in response to oxidative and abiotic stress in rice.展开更多
Increase uric acid levels have been found in oxidative stress. Urate radicals do not react with oxygen to form another peroxy radical, thus increasing the efficacy of uric acid as an antioxidant. Therefore, this study...Increase uric acid levels have been found in oxidative stress. Urate radicals do not react with oxygen to form another peroxy radical, thus increasing the efficacy of uric acid as an antioxidant. Therefore, this study is designed to measure the level of uric acids and find out the relationship of uric acid with superoxide dismutase in induced hyperuricemic model. Forty male albino rats with an average weight of 180 ± 2 g were selected. The rats were grouped. The animals were fed on standard diet and given tap water ad libitum until treatment. Albino rats were divided into four groups. Group A(10)-control given only standard diet, group B(10) fed on 60% fructose with standard diet , group C(10) fed on fructose, standard diet and intraperitonially oxonic acid 250 mg/kg and group D (10) only on injection intraperotonially oxonic acid 250 mg/kg. At the end of study 10 mL of blood was drawn from heart of rats. Then blood was estimated for superoxide dismutase and uric acids done by kit methods randox-manual/Rx monza UA230/UA 233. Results: In Group C superoxide dismutase was found to be 32 % (244 mg/dL ± 2.23) more than control. In the same group the uric acid concentration was highly significantly correlated with control. Conclusion: The uric acid concentration increases when we take fructose up to 60% in our diet. It also increases superoxide dismutase concentration. More than this value may have inverse effect on the uric acid level and its role as an antioxidant may become inversed.展开更多
AIM: To evaluate αB-crystallin malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) changes in X-ray irradiated rat lens. METHODS: Eight-week-old Sprague-Dawley male rats received X-ray ...AIM: To evaluate αB-crystallin malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) changes in X-ray irradiated rat lens. METHODS: Eight-week-old Sprague-Dawley male rats received X-ray irradiation to the head with rest of the body protected. The exposure dose ranged from 2 to 25 Grays (Gy). The cataract status were examined by slit lamp and rated with "four-grade systems" post-irradiation. The lens MDA level, and the activities of SOD and GPx were measured in a short-term experiment post-irradiation, and αB-crystallin protein levels were quantified. RESULTS: The lenses of normal control and the X-ray irradiated groups with the dose up to 10 Gy remained transparent throughout the experiment. The lens first appeared tiny scatters, and even lamellar opacities in the posterior capsule 45 days post-irradiation with the dose of 15 Gy, and progressed slowly to the advance stage of cataract; while, for the higher dose (25 Gy), the opacity of lens appeared much earlier, and progressed more rapidly to mature stage of cataract within 1 month. At the end of the observation (90 days post-irradiation), almost all lenses became complete opacity with the higher dose (25 Gy). The degree of lens opacity was rated accordingly. The lens MDA level was increased, and SOD and GPx activities were decreased with a dose-dependent manner post-irradiation. The αB-crystallin protein level was decreased dose-dependently at the end point of observation. CONCLUSION: Oxidative events and αB-crystallin may play important roles in the pathogenesis of cataract in X-ray irradiated rat lens.展开更多
文摘目的研究程序性细胞死亡蛋白4(programmed cell death protein 4,PDCD4)在脓毒症诱导的急性肾损伤(acute kidney injury,AKI)中的作用机制,以及调控PDCD4表达通过丝裂原活化蛋白激酶3(mitogen-activated protein kinase 3,MAP2K3)和p38蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)对脓毒症AKI起到潜在治疗作用。方法用脂多糖(lipopolysaccharide,LPS)刺激人肾小管上皮细胞(HK-2)构建脓毒症AKI细胞模型。进一步用腺病毒介导siRNA和过表达载体抑制和上调AKI细胞模型中PDCD4的表达;CCK-8法检测细胞增殖;用DCFH-DA及激光共聚焦显微镜检测细胞中ROS水平,用总SOD活性检测试剂和MDA检测试剂盒检测细胞中SOD和MDA水平;免疫共沉淀验证PDCD4和MAP2K3之间的蛋白相互作用;TUNEL染色法检测细胞凋亡;RT-qPCR和Western blot检测PDCD4及相关基因的mRNA和蛋白表达水平;ELISA法检测患者血清中炎症相关因子水平。结果LPS诱导可以促进HK-2细胞中PDCD4表达,下调PDCD4可抑制LPS诱导的HK-2细胞的炎症、氧化应激及细胞凋亡。数据库预测及免疫共沉淀证实PDCD4可以与MAP2K3相互作用,且在LPS诱导的HK-2细胞中,MAP2K3表达水平显著增强。MAP2K3过表达和p38 MAPK激动剂可以减轻PDCD4下调对LPS诱导的细胞炎症和氧化应激的影响并抑制细胞凋亡。结论下调PDCD4可以通过抑制MAP2K3和p38 MAPK从而抑制LPS诱导的肾小管上皮细胞的炎症和凋亡。
文摘Although mutations in the superoxide dismutase 1 gene account for only a minority of total amyotrophic lateral sclerosis cases,the discovery of this gene has been crucial for amyotrophic lateral sclerosis research.Since the identification of superoxide dismutase 1 in 1993,the field of amyotrophic lateral sclerosis genetics has considerably widened,improving our understanding of the diverse pathogenic basis of amyotrophic lateral sclerosis.In this review,we focus on cognitive impairment in superoxide dismutase 1-amyotrophic lateral sclerosis patients.Literature has mostly reported that cognition remains intact in superoxide dismutase 1-amyotrophic lateral sclerosis patients,but recent reports highlight frontal lobe function frailty in patients carrying different superoxide dismutase 1-amyotrophic lateral sclerosis mutations.We thoroughly reviewed all the various mutations reported in the literature to contribute to a comprehensive database of superoxide dismutase 1-amyotrophic lateral sclerosis genotype-phenotype correlation.Such a resource could ultimately improve our mechanistic understanding of amyotrophic lateral sclerosis,enabling a more robust assessment of how the amyotrophic lateral sclerosis phenotype responds to different variants across genes,which is important for the therapeutic strategy targeting genetic mutations.Cognition in superoxide dismutase 1-amyotrophic lateral sclerosis deserves further longitudinal research since this peculiar frailty in patients with similar mutations can be conditioned by external factors,including environment and other unidentified agents including modifier genes.
基金supported by a grant from the Association Française contre les Myopathies(AFM Téléthongrant 23667,to JCL).
文摘Amyotrophic lateral sclerosis is a very disabling disease due to the degeneration of motor neurons.Symptoms include muscle weakness and atrophy,spasticity,and progressive paralysis.Currently,there is no treatment to reverse damage to motor neurons and cure amyotrophic lateral sclerosis.The only two treatments actually approved,riluzole and edaravone,have shown mitigated beneficial effects.The difficulty to find a cure lies in the complexity and multifaceted pattern of amyotrophic lateral sclerosis pathogenesis.Among mechanisms,abnormal RNA metabolism,nucleocytoplasmic transport defects,accumulation of unfolded protein,and mitochondrial dysfunction would in fine induce oxidative damage and vice versa.A potent therapeutic strategy will be to find molecules that break this vicious circle.Sharpening the nuclear factor erythroid-2 related factor 2 signaling may fulfill this objective since nuclear factor erythroid-2 related factor 2 has a multitarget profile controlling antioxidant defense,mitochondrial functioning,and inflammation.We here discuss the interest of developing nuclear factor erythroid-2 related factor 2-based therapy in regard to the pathophysiological mechanisms and we provide a general overview of the attempted clinical assays in amyotrophic lateral sclerosis.
文摘Objective To investigate the correlation between drinking behavior combined with polymorphisms of extracellular superoxide dismutase(EC-SOD) and aldehyde dehydrogenase-2(ALDH2) genes and pancreatic cancer. Methods The genetic polymorphisms of EC-SOD and ALDH2 were analyzed by polymerase chain reaction restriction fragment length polymorphism in the peripheral blood leukocytes obtained from 680 pancreatic cancer cases and 680 non-cancer controls. Subsequently the frequency of genotype was compared between the pancreatic cancer patients and the healthy controls.The relationship of drinking with pancreatic cancer was analyzed. Results The frequencies of EC-SOD(C/G) and ALDH2 variant genotypes were 37.35% and 68.82% respectively in the pancreatic cancer cases, and were significantly higher than those in the healthy controls(21.03% and 44.56%, all P<0.01). People who carried EC-SOD(C/G)(OR=2.24, 95% CI= 1.81-4.03, P<0.01) or ALDH2 variant genotypes(OR=2.75, 95% CI=1.92-4.47, P<0.01) had a high risk to develop pancreatic cancer. Those who carried EC-SOD(C/G) genotype combined with ALDH2 variant genotype had a high risk for pancreatic cancer(29.56% vs. 6.76%, OR=7.69, 95% CI=3.58-10.51, P<0.01). The drinking rate of the pancreatic cancer group(64.12%) was significantly higher than that of the control group(40.15%; OR=2.66, 95% CI=1.30-4.42, P<0.01). An interaction between drinking and EC-SOD(C/G)/ALDH2 variant genotypes increased the risk of occurrence of pancreatic cancer(OR=25.00, 95% CI= 11.87-35.64, P<0.01). Conclusion EC-SOD(C/G), ALDH2 variant genotypes and drinking might be the risk factors of pancreatic cancer.
基金funded by the Special Fund for Agro-scientific Research in the Public Industry of China (201203085 )the Fundamental Research Fund of Central Welfare Scientific Research Institutes (201003)
文摘[Objective]This study was to investigate the effect of different concentrations of Norfloxacin on the superoxide dismutase ( SOD) activities in the blood plasma and liver tissues of Amur sturgeon ( Acipenser schrencki Brandt) and sterlet ( Acipenser ruthenus Linnaeus) . [Method] Using pharmaco-toxicological evaluation method,Norfloxacin with the concentrations of 0,20,40,60,80 and 100 mg /kg,was orally delivered to the Amur sturgeon and sterlet for 5 d,respectively. The SOD activities in the blood plasma and liver tissues were measured after drug withdrawal for 2 d to explore the optimal dosing concentration of Norfloxacin during sturgeon culture,as well as the effect of Norfloxacin on liver injury. [Result] SOD existed in both two sturgeons but with different amounts,and the SOD activities were higher in the livers than in the blood plasma no matter in the control and all drug delivered groups. Under different drug delivery concentrations,the SOD activities first increased and then decreased in the 2 tissues of the 2 sturgeon species,and the SOD activities reached the maximum when the drug delivery concentration was 40 mg /kg. The drug de- livery concentration had little effect on the SOD activities in the blood plasma,which showed stable changes. When the drug delivery concentration was 40 mg /kg,the SOD activities in the blood plasma of Amur sturgeon were higher than that of sterlet,while for the other concentrations,the SOD activities in the plasma of sterlet showed higher performance. However,the SOD activities changed significantly through drug delivery in the liver tis- sues,and the SOD activities were higher in the sterlet than in the Amur sturgeon when the drug delivery concentrations were 0,40 and 100 mg /kg. The SOD activity in the sterlet was the highest under 40 mg /kg,presenting a sharp peak value. The optimal drug delivery concentration of Norfloxa- cin was 30 -50 mg /kg,under which the Norfloxacin presented best effect and had no injury effect on livers. [Conclusion]This study provides theo- retical basis for the reasonable application of Norfloxacin in aquaculture.
基金supported by the Grants-in-Aid for Scientific Research (Grant No. 10460149 to K.T. and Grant No. 11740448 to S.M.) from the Ministry of Education, Culture, Sports, Science and Technology of Japana grant from the Rice Genome Research Program (Grant No. MP2106 to K.T.) from the Ministry of Agriculture, Forestry and Fisheries of Japan
文摘Superoxide dismutase (SOD) and ascorbate peroxidase (APX) play central roles in the pathway for scavenging reactive oxygen species in plants, thereby contributing to the tolerance against abiotic stress. Here we report the responses of cytosolic SOD (cSOD; sodCc1 and sodCc2) and cytosolic APX (cAPX; OsAPX1 and OsAPX2) genes to oxidative and abiotic stress in rice. RNA blot analyses revealed that methyl viologen treatment caused a more prominent induction of cAPXs compared with cSODs, and hydrogen peroxide treatment induced the expression of cAPXs whereas cSODs were not affected. These results suggest that cAPXs play more important roles in defense against oxidative stress compared with cSODs. It is noted that cSODs and cAPXs showed coordinate response to abscisic acid treatment which induced both sodCc1 and OsAPX2. However, cSODs and cAPXs responded differentially to drought, salt and chilling stress, which indicates that cSOD and cAPX genes are expressed differentially in response to oxidative and abiotic stress in rice.
文摘Increase uric acid levels have been found in oxidative stress. Urate radicals do not react with oxygen to form another peroxy radical, thus increasing the efficacy of uric acid as an antioxidant. Therefore, this study is designed to measure the level of uric acids and find out the relationship of uric acid with superoxide dismutase in induced hyperuricemic model. Forty male albino rats with an average weight of 180 ± 2 g were selected. The rats were grouped. The animals were fed on standard diet and given tap water ad libitum until treatment. Albino rats were divided into four groups. Group A(10)-control given only standard diet, group B(10) fed on 60% fructose with standard diet , group C(10) fed on fructose, standard diet and intraperitonially oxonic acid 250 mg/kg and group D (10) only on injection intraperotonially oxonic acid 250 mg/kg. At the end of study 10 mL of blood was drawn from heart of rats. Then blood was estimated for superoxide dismutase and uric acids done by kit methods randox-manual/Rx monza UA230/UA 233. Results: In Group C superoxide dismutase was found to be 32 % (244 mg/dL ± 2.23) more than control. In the same group the uric acid concentration was highly significantly correlated with control. Conclusion: The uric acid concentration increases when we take fructose up to 60% in our diet. It also increases superoxide dismutase concentration. More than this value may have inverse effect on the uric acid level and its role as an antioxidant may become inversed.
基金Scientific Research Foundation for Returned Scholars, the Second Hospital Affiliated to Soochow University (No.SDFEY-2007-10)National Natural Science Foundation of China (No.81000383)+2 种基金Research Fund for the Doctoral Program of Higher Education of China (No.20100072120051)Program of Tongji University (No.1500219024 No.2010QH04 and No. 2010YF02)
文摘AIM: To evaluate αB-crystallin malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) changes in X-ray irradiated rat lens. METHODS: Eight-week-old Sprague-Dawley male rats received X-ray irradiation to the head with rest of the body protected. The exposure dose ranged from 2 to 25 Grays (Gy). The cataract status were examined by slit lamp and rated with "four-grade systems" post-irradiation. The lens MDA level, and the activities of SOD and GPx were measured in a short-term experiment post-irradiation, and αB-crystallin protein levels were quantified. RESULTS: The lenses of normal control and the X-ray irradiated groups with the dose up to 10 Gy remained transparent throughout the experiment. The lens first appeared tiny scatters, and even lamellar opacities in the posterior capsule 45 days post-irradiation with the dose of 15 Gy, and progressed slowly to the advance stage of cataract; while, for the higher dose (25 Gy), the opacity of lens appeared much earlier, and progressed more rapidly to mature stage of cataract within 1 month. At the end of the observation (90 days post-irradiation), almost all lenses became complete opacity with the higher dose (25 Gy). The degree of lens opacity was rated accordingly. The lens MDA level was increased, and SOD and GPx activities were decreased with a dose-dependent manner post-irradiation. The αB-crystallin protein level was decreased dose-dependently at the end point of observation. CONCLUSION: Oxidative events and αB-crystallin may play important roles in the pathogenesis of cataract in X-ray irradiated rat lens.
