Inborn and induced defects of the mitochondrial respiratory chain.
نویسندگان
چکیده
996 19 Katsura, K., Minamisawa. H., Ekholm. A., Folbergrova, J. and Siesjii, H. K. ( 1 992) Hrain Res. 590,6I 2 20 Ekholm. A,, Katsura. K. and Siesjii, H. K. (lOO3) J. Cereb. Hlood Flow Metab. 13, 193-200 21 Kristian, T., Katsura. K., Gid6. G. and Siesjo. H. K. (1904) Hrain Res. 641.295-302 22 Ou-Yang. Y.. Kristian, T., Mellergird. 1’. and Siesjo. H. K. (1994) Hrain Res. 646,hS-72 23 I’umain, R. and tleinemann, I T . (1985) J. Neurophysiol. 53. 1 16 24 Kocher. M. (1990) J. Cereb. Hlood Flow Metab. 10. 564-571 25 Gidii, G., Katsura, K.. Kristiin. T. and Siesjo. H. K. (1903) J. Cereb. Hlood Flow Metab. 13, 179-182 20 Wieloch, T., liarris, R. J.. Symon, I,. and Siesjii. H. K. ( 1984) J. Neurochem. 43. 160168 27 Silver. I . A. and Ereciiiska. M. (1902) J. Cereb. Hlood Flow Metab. 12,759-772 28 Floyd. R. ( 1990) FASEH J. 4,2587-2507 29 Halliwell. H. (1992) J. Neurochem. 59. 1609-1623 30 Ekholm. A,, Katsura. K.. Kristian, T.. I,iu. M.. Folbergrova, J. and Siesjo, H. K. (1993) Hrain Res. 604, 1 85 1 0 1 31 Chapman, A. G.. Westerberg, E. V. and Siesjii. H. K. ( 198 I ) J. Neurochem. 36. 170189 32 Kleihues. I’.. Kobayashi. K. and I lossmann, K.-A. (1074) J. Neurochem. 23.4 17-425 33 Katsura. K., Hengrsson. F.. Ekholm, A., Kristian, T.. (hsdii. G. and Siesjij. H. K. (1003) J. Cereb. Hlood Flow Metab. 13. 820-820
منابع مشابه
Long-term, high-dose aspirin therapy increases the specific activity of complex III of mitochondrial respiratory chain in the kidney of diabetic rats
Introduction: One of the main mechanisms by which diabetic complications occur is an alteration of the structure and function of proteins due to hyperglycemia. Aspirin (ASA) affects cellular pathways through different mechanisms, including glycation inhibition and antioxidant activity. The aim of the present study, as a follow up to our previous one, is to investigate the effect of long-term, h...
متن کاملجهش جدید هموپلاسمیک T4216C میتوکندریایی در افراد ایرانی مبتلا به بیماری فردریش اتاکسیا
Introduction: The mitochondrial defects in Friedreich ataxia (FRDA) have been reported in many researches. Friedreich ataxia is an autosomal recessive neurodegenerative disorder caused by decreased expression of the Frataxin protein. Frataxin deficiency leads to excessive free radical production and dysfunction of respiratory chain complexes. Mitochondrial DNA (mtDNA) could be considered as a c...
متن کاملToxicity mechanisms of Cigarette Smoke on Eye and Kidney using Isolated Mitochondria
Cigarette smoking is one of the main risk factors for premature human death associated to a variety of respiratory and vascular diseases, and cancer due to containing Hundreds of toxicants. Rat mitochondria were obtained by differential ultracentrifugation and incubated with different concentrations (1, 10 and 100%) of standardized cigarette smoke extract (CSE). Our results showed that cigarett...
متن کاملشناسایی یک حذف بزرگ در DNA میتوکندریایی بیماران ایرانی مبتلا به آریتمی قلبی
Introduction: Long QT Syndrome is one of the arrhythmic disorders of the heart that causes sudden cardiac death in patients. Most of the investigations have focused on nuclear genome for finding genetic defects in these disorders, but some of the cases with LQTS cannot be explained by mutations of identified genes. It prompted the authors to focus on the mitochondrial DNA and monitor rearrangem...
متن کاملInvolvement of Four Different Intracellular Sites in Chloroacetaldehyde- Induced Oxidative Stress Cytotoxicity
Chloroacetaldehyde (CAA) is a chlorination by-product in finished drinking water and a toxic metabolite of a wide variety of industrial chemicals (e.g. vinyl chloride) and chemotherapeutic agents (e.g. cyclophosphamide and ifosfamide). In this research, the cytotoxic mechanisms of CAA in freshly isolated rat hepatocytes were investigated.CAA cytotoxicity was associated with reactive oxygen spec...
متن کاملInvolvement of Four Different Intracellular Sites in Chloroacetaldehyde- Induced Oxidative Stress Cytotoxicity
Chloroacetaldehyde (CAA) is a chlorination by-product in finished drinking water and a toxic metabolite of a wide variety of industrial chemicals (e.g. vinyl chloride) and chemotherapeutic agents (e.g. cyclophosphamide and ifosfamide). In this research, the cytotoxic mechanisms of CAA in freshly isolated rat hepatocytes were investigated.CAA cytotoxicity was associated with reactive oxygen spec...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Biochemical Society transactions
دوره 22 4 شماره
صفحات -
تاریخ انتشار 1994