{"title":"葡萄糖-6-磷酸脱氢酶缺乏症患者总抗氧化活性的研究","authors":"A. Palasuwan, S. Soogarun, V. Wiwanitkit","doi":"10.5580/1821","DOIUrl":null,"url":null,"abstract":"Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common inherited enzyme deficiency. This disorder causes hemolytic anemia, which is often enhanced by an identifiable chemical trigger or infection [1,2]. G6PD is the key rate-limiting enzyme in the pentose pathway and the expression of its gene has been shown to be redox-sensitive [3] Physiologically, G6PD plays an important role in cellular redox homeostasis, which is crucial for cell survival [4]. Cheng et al said that G6PD status determined the response of cells exposed to nitric oxide (NO) donor [4]. Overexpression of G6PD in vascular endothelial cells decreases reactive oxygen species accumulation in response to exogenous and endogenous oxidant stress and improves levels of bioavailable NO [5]. Here the authors investigated the antioxidant activity in a sample of healthy subjects comparing to subjects with G6PD deficiency. A total of 21 volunteer subjects were included into this investigation. All were screened for the G6PD deficiency by a biochemical assay kit 345 – A, (Sigma Co.) and 2 were detected to have G6PD deficiency. All were studied for the antioxidant activity by the Trolox equivalent antioxidant capacity (TEAC) method []. The average antioxidant activity in the healthy subjects and subjects with G6PD deficiency are 3.35 ± 0.27 mM Trolox equivalent and 3.17 ± 0.05 mM Trolox equivalent respectively. It seems that the antioxidant level in the subjects with G6PD deficiency might not different from the healthy subjects. However, the number of subjects in this study is rather few. Further larger study is recommended before final conclusion.","PeriodicalId":331725,"journal":{"name":"The Internet Journal of Tropical Medicine","volume":"33 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2004-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A Note On The Total Antioxidant Activity In The Subjects With Glucose-6-Phosphate Dehydrogenase Deficiency\",\"authors\":\"A. Palasuwan, S. Soogarun, V. Wiwanitkit\",\"doi\":\"10.5580/1821\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common inherited enzyme deficiency. This disorder causes hemolytic anemia, which is often enhanced by an identifiable chemical trigger or infection [1,2]. G6PD is the key rate-limiting enzyme in the pentose pathway and the expression of its gene has been shown to be redox-sensitive [3] Physiologically, G6PD plays an important role in cellular redox homeostasis, which is crucial for cell survival [4]. Cheng et al said that G6PD status determined the response of cells exposed to nitric oxide (NO) donor [4]. Overexpression of G6PD in vascular endothelial cells decreases reactive oxygen species accumulation in response to exogenous and endogenous oxidant stress and improves levels of bioavailable NO [5]. Here the authors investigated the antioxidant activity in a sample of healthy subjects comparing to subjects with G6PD deficiency. A total of 21 volunteer subjects were included into this investigation. All were screened for the G6PD deficiency by a biochemical assay kit 345 – A, (Sigma Co.) and 2 were detected to have G6PD deficiency. All were studied for the antioxidant activity by the Trolox equivalent antioxidant capacity (TEAC) method []. The average antioxidant activity in the healthy subjects and subjects with G6PD deficiency are 3.35 ± 0.27 mM Trolox equivalent and 3.17 ± 0.05 mM Trolox equivalent respectively. It seems that the antioxidant level in the subjects with G6PD deficiency might not different from the healthy subjects. However, the number of subjects in this study is rather few. Further larger study is recommended before final conclusion.\",\"PeriodicalId\":331725,\"journal\":{\"name\":\"The Internet Journal of Tropical Medicine\",\"volume\":\"33 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2004-12-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Internet Journal of Tropical Medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5580/1821\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Internet Journal of Tropical Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5580/1821","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
葡萄糖-6-磷酸脱氢酶(G6PD)缺乏是一种常见的遗传性酶缺乏症。这种疾病会导致溶血性贫血,可识别的化学触发或感染通常会加重溶血性贫血[1,2]。G6PD是戊糖通路中关键的限速酶,其基因表达具有氧化还原敏感性[3],在生理上,G6PD在细胞氧化还原稳态中起重要作用,对细胞存活至关重要[4]。Cheng等认为G6PD状态决定了细胞暴露于一氧化氮(NO)供体后的反应[4]。血管内皮细胞中G6PD的过表达减少了响应外源性和内源性氧化应激的活性氧积累,提高了生物可利用NO水平[5]。在这里,作者研究了健康受试者与G6PD缺乏症受试者的抗氧化活性。共有21名志愿者参与了本次调查。所有人都通过生化检测试剂盒345 - a (Sigma Co.)筛选G6PD缺乏症,其中2人被检测为G6PD缺乏症。采用Trolox等效抗氧化能力(TEAC)法研究了所有化合物的抗氧化活性[]。健康组和G6PD缺乏症组的平均抗氧化活性分别为3.35±0.27 mM Trolox当量和3.17±0.05 mM Trolox当量。G6PD缺乏症患者体内抗氧化水平与健康人群无明显差异。然而,本研究的受试者数量很少。建议在最终结论之前进行更大规模的研究。
A Note On The Total Antioxidant Activity In The Subjects With Glucose-6-Phosphate Dehydrogenase Deficiency
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common inherited enzyme deficiency. This disorder causes hemolytic anemia, which is often enhanced by an identifiable chemical trigger or infection [1,2]. G6PD is the key rate-limiting enzyme in the pentose pathway and the expression of its gene has been shown to be redox-sensitive [3] Physiologically, G6PD plays an important role in cellular redox homeostasis, which is crucial for cell survival [4]. Cheng et al said that G6PD status determined the response of cells exposed to nitric oxide (NO) donor [4]. Overexpression of G6PD in vascular endothelial cells decreases reactive oxygen species accumulation in response to exogenous and endogenous oxidant stress and improves levels of bioavailable NO [5]. Here the authors investigated the antioxidant activity in a sample of healthy subjects comparing to subjects with G6PD deficiency. A total of 21 volunteer subjects were included into this investigation. All were screened for the G6PD deficiency by a biochemical assay kit 345 – A, (Sigma Co.) and 2 were detected to have G6PD deficiency. All were studied for the antioxidant activity by the Trolox equivalent antioxidant capacity (TEAC) method []. The average antioxidant activity in the healthy subjects and subjects with G6PD deficiency are 3.35 ± 0.27 mM Trolox equivalent and 3.17 ± 0.05 mM Trolox equivalent respectively. It seems that the antioxidant level in the subjects with G6PD deficiency might not different from the healthy subjects. However, the number of subjects in this study is rather few. Further larger study is recommended before final conclusion.