Calcium-dependent mitochondrial permeability transition is augmented in the kidney of Goto-Kakizaki diabetic rat
Background Renal disease associated with diabetes mellitus is a major problem among diabetic patients. The role of mitochondria in the pathogenesis of diabetes has received a large amount of attention in the last years, but many aspects of this subject are still poorly understood. In the present stu...
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| Published in | Diabetes/metabolism research and reviews Vol. 20; no. 2; pp. 131 - 136 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Chichester, UK
John Wiley & Sons, Ltd
01.03.2004
Wiley |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1520-7552 1520-7560 |
| DOI | 10.1002/dmrr.423 |
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| Abstract | Background
Renal disease associated with diabetes mellitus is a major problem among diabetic patients. The role of mitochondria in the pathogenesis of diabetes has received a large amount of attention in the last years, but many aspects of this subject are still poorly understood. In the present study, we studied the susceptibility of the mitochondrial permeability transition (MPT) on kidney mitochondria from the Goto‐Kakizaki (GK) rat, an animal model featuring physiological and pathological alterations characteristic of type 2 diabetes.
Methods
Kidney mitochondria were isolated by differential centrifugations; mitochondrial electric transmembrane potential and calcium loading capacity were evaluated with a TPP+‐selective electrode and with a calcium‐sensitive fluorescent probe. Coenzyme Q9, Q10 and vitamin E were evaluated by high‐performance liquid chromatography (HPLC).
Results
Kidney mitochondria from the diabetic animals had an increased susceptibility to the induction of the MPT by calcium. We observed a loss of calcium‐loading capacity and a higher calcium‐induced mitochondrial depolarization. Vitamin E and coenzyme Q9 were also increased in kidney mitochondria from GK rats.
Conclusions
The results show an enhanced MPT activation in kidney mitochondria from GK rats, which lead us to suggest that this condition may be one major alteration triggered by chronic diabetes in kidney cells, ultimately leading to cell dysfunction. Copyright © 2004 John Wiley & Sons, Ltd. |
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| AbstractList | Background Renal disease associated with diabetes mellitus is a major problem among diabetic patients. The role of mitochondria in the pathogenesis of diabetes has received a large amount of attention in the last years, but many aspects of this subject are still poorly understood. In the present study, we studied the susceptibility of the mitochondrial permeability transition (MPT) on kidney mitochondria from the Goto-Kakizaki (GK) rat, an animal model featuring physiological and pathological alterations characteristic of type 2 diabetes. Methods Kidney mitochondria were isolated by differential centrifugations; mitochondrial electric transmembrane potential and calcium loading capacity were evaluated with a TPP+-selective electrode and with a calcium-sensitive fluorescent probe. Coenzyme Q9, Q10 and vitamin E were evaluated by high-performance liquid chromatography (HPLC). Results Kidney mitochondria from the diabetic animals had an increased susceptibility to the induction of the MPT by calcium. We observed a loss of calcium-loading capacity and a higher calcium-induced mitochondrial depolarization. Vitamin E and coenzyme Q9 were also increased in kidney mitochondria from GK rats. Conclusions The results show an enhanced MPT activation in kidney mitochondria from GK rats, which lead us to suggest that this condition may be one major alteration triggered by chronic diabetes in kidney cells, ultimately leading to cell dysfunction. Background Renal disease associated with diabetes mellitus is a major problem among diabetic patients. The role of mitochondria in the pathogenesis of diabetes has received a large amount of attention in the last years, but many aspects of this subject are still poorly understood. In the present study, we studied the susceptibility of the mitochondrial permeability transition (MPT) on kidney mitochondria from the Goto‐Kakizaki (GK) rat, an animal model featuring physiological and pathological alterations characteristic of type 2 diabetes. Methods Kidney mitochondria were isolated by differential centrifugations; mitochondrial electric transmembrane potential and calcium loading capacity were evaluated with a TPP+‐selective electrode and with a calcium‐sensitive fluorescent probe. Coenzyme Q9, Q10 and vitamin E were evaluated by high‐performance liquid chromatography (HPLC). Results Kidney mitochondria from the diabetic animals had an increased susceptibility to the induction of the MPT by calcium. We observed a loss of calcium‐loading capacity and a higher calcium‐induced mitochondrial depolarization. Vitamin E and coenzyme Q9 were also increased in kidney mitochondria from GK rats. Conclusions The results show an enhanced MPT activation in kidney mitochondria from GK rats, which lead us to suggest that this condition may be one major alteration triggered by chronic diabetes in kidney cells, ultimately leading to cell dysfunction. Copyright © 2004 John Wiley & Sons, Ltd. Renal disease associated with diabetes mellitus is a major problem among diabetic patients. The role of mitochondria in the pathogenesis of diabetes has received a large amount of attention in the last years, but many aspects of this subject are still poorly understood. In the present study, we studied the susceptibility of the mitochondrial permeability transition (MPT) on kidney mitochondria from the Goto-Kakizaki (GK) rat, an animal model featuring physiological and pathological alterations characteristic of type 2 diabetes. Kidney mitochondria were isolated by differential centrifugations; mitochondrial electric transmembrane potential and calcium loading capacity were evaluated with a TPP+-selective electrode and with a calcium-sensitive fluorescent probe. Coenzyme Q9, Q10 and vitamin E were evaluated by high-performance liquid chromatography (HPLC). Kidney mitochondria from the diabetic animals had an increased susceptibility to the induction of the MPT by calcium. We observed a loss of calcium-loading capacity and a higher calcium-induced mitochondrial depolarization. Vitamin E and coenzyme Q9 were also increased in kidney mitochondria from GK rats. The results show an enhanced MPT activation in kidney mitochondria from GK rats, which lead us to suggest that this condition may be one major alteration triggered by chronic diabetes in kidney cells, ultimately leading to cell dysfunction. Renal disease associated with diabetes mellitus is a major problem among diabetic patients. The role of mitochondria in the pathogenesis of diabetes has received a large amount of attention in the last years, but many aspects of this subject are still poorly understood. In the present study, we studied the susceptibility of the mitochondrial permeability transition (MPT) on kidney mitochondria from the Goto-Kakizaki (GK) rat, an animal model featuring physiological and pathological alterations characteristic of type 2 diabetes.BACKGROUNDRenal disease associated with diabetes mellitus is a major problem among diabetic patients. The role of mitochondria in the pathogenesis of diabetes has received a large amount of attention in the last years, but many aspects of this subject are still poorly understood. In the present study, we studied the susceptibility of the mitochondrial permeability transition (MPT) on kidney mitochondria from the Goto-Kakizaki (GK) rat, an animal model featuring physiological and pathological alterations characteristic of type 2 diabetes.Kidney mitochondria were isolated by differential centrifugations; mitochondrial electric transmembrane potential and calcium loading capacity were evaluated with a TPP+-selective electrode and with a calcium-sensitive fluorescent probe. Coenzyme Q9, Q10 and vitamin E were evaluated by high-performance liquid chromatography (HPLC).METHODSKidney mitochondria were isolated by differential centrifugations; mitochondrial electric transmembrane potential and calcium loading capacity were evaluated with a TPP+-selective electrode and with a calcium-sensitive fluorescent probe. Coenzyme Q9, Q10 and vitamin E were evaluated by high-performance liquid chromatography (HPLC).Kidney mitochondria from the diabetic animals had an increased susceptibility to the induction of the MPT by calcium. We observed a loss of calcium-loading capacity and a higher calcium-induced mitochondrial depolarization. Vitamin E and coenzyme Q9 were also increased in kidney mitochondria from GK rats.RESULTSKidney mitochondria from the diabetic animals had an increased susceptibility to the induction of the MPT by calcium. We observed a loss of calcium-loading capacity and a higher calcium-induced mitochondrial depolarization. Vitamin E and coenzyme Q9 were also increased in kidney mitochondria from GK rats.The results show an enhanced MPT activation in kidney mitochondria from GK rats, which lead us to suggest that this condition may be one major alteration triggered by chronic diabetes in kidney cells, ultimately leading to cell dysfunction.CONCLUSIONSThe results show an enhanced MPT activation in kidney mitochondria from GK rats, which lead us to suggest that this condition may be one major alteration triggered by chronic diabetes in kidney cells, ultimately leading to cell dysfunction. |
| Author | Seiça, Raquel Moreno, António J. M. Oliveira, Paulo J. Esteves, Telma C. Santos, Maria S. |
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| Cites_doi | 10.1002/biof.5520090215 10.1016/S0014-5793(01)02316-X 10.1042/bj3410233 10.1054/ceca.1999.0076 10.1016/S0076-6879(84)05020-5 10.1023/A:1010482017540 10.1079/PNS19970029 10.1002/dmrr.200 10.1016/0304-3940(93)90582-6 10.1042/bj1920853 10.1023/A:1023475022025 10.1002/biof.5520080315 10.1016/S0021-9258(18)83116-7 10.1007/BF01868720 10.1016/S0024-3205(00)00892-4 10.1006/bbrc.1996.0776 |
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| Keywords | Endocrinopathy Type 2 diabetes Animal model Mitochondria Goto-Kakizaki rat Calcium kidney mitochondria mitochondrial permeability transition Permeability Inorganic element Kidney Goto Kakizaki rat |
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| References | Broekemeier KM, Dempsey ME, Pfeiffer DR. Cyclosporin A Is a Potent Inhibitor of the inner membrane mitochondrial transition in liver mitochondria. J Biol Chem 1989; 264: 7826-7830. Santos MS, Duarte AI, Matos MJ, Proenca T, Seica R, Oliveira CR. Synaptosomes isolated from Goto-Kakizaki diabetic rat brain exhibit increased resistance to oxidative stress: role of vitamin E. Life Sci 2000; 67(25): 3061-3073. Oliveira PJ, Rolo AP, Seiça R, Palmeira CP, Santos MS, Moreno AJ. Decreased susceptibility of heart mitochondria from diabetic GK rats to mitochondrial permeability transition induced by calcium/phosphate. Biosci Rep 2001; 21: 55-62. Takada M, Ikenoya S, Yuzuriha T, Katayama K. Simultaneous determination of reduced and oxidized ubiquinones. Methods Enzymol 1984; 105: 147-155. Rizzuto R, Pinton P, Brini M, Chiesa A, Filippin L, Pozzan T. Mitochondria as biosensors of calcium microdomains. Cell Calcium 1999; 26: 193-199. Takayanagi R, Takeshige T, Minakami P. NADH- and NADPH-dependent lipid peroxidation in bovine submitochondrial particles. Biochem J 1980; 192: 853-860. Crompton M. The mitochondrial permeability transition pore and its role in cell death. Biochem J 1999; 341: 233-249. Santos DL, Palmeira CM, Seica R, et al. Diabetes and mitochondrial oxidative stress: a study using heart mitochondria from the diabetic Goto-Kakizaki rat. Mol Cell Biochem 2003; 246(1-2): 163-170. Kamo N, Muratsugu M, Hongoh R, Kobatake Y. Membrane potential of mitochondria measured with an electrode sensitive to tetraphenyl phosphonium and relationship between proton electrochemical potential and phosphorylation potential in steady state. J Membr Biol 1979; 49: 105-121. Rajdev S, Reynolds IJ. Calcium Green-5N, a novel fluorescent probe for monitoring high intracellular free Ca2+ concentrations associated with glutamate excitotoxicity in cultured rat brain neurons. Neurosci Lett 1993; 162: 149-152. Kristal BS, Matsuda M, Yu BP. Abnormalities in the mitochondrial permeability transition in diabetic rats. Biochem Biophys Res Commun 1996; 222: 519-523. Kowaltowski AJ, Castilho RF, Vercesi AE. Mitochondrial permeability transition and oxidative stress. FEBS Lett 2001; 495: 12-15. Santos MS, Santos DL, Palmeira CM, Seica R, Moreno AJ, Oliveira CR. Brain and liver mitochondria isolated from diabetic Goto-Kakizaki rats show different susceptibility to induced oxidative stress. Diabetes Metab Res Rev 2001; 17(3): 223-230. Bernardi P, Colonna R, Costantini P, et al. The mitochondrial permeability transition. Biofactors 1998; 8: 273-281. Flatt P, Abdel-Wahab Y, Boyd AC. Pancreatic B-cell dysfunction and glucose toxicity in non-insulin-dependent diabetes. Proc Nutr Soc 1997; 56: 243-262. Lass A, Kwong L, Sohal RS. Mitochondrial coenzyme Q content and aging. Biofactors 1999; 9: 199-205. 1979; 49 2001; 495 1990 2000; 67 1989; 264 1984; 105 1999; 26 1997; 56 1998 1999; 341 1993; 162 1980; 192 2001; 17 2003; 246 1996; 222 1998; 8 1999; 9 2001; 21 Goto Y (e_1_2_6_7_2) 1998 Pinto JR (e_1_2_6_3_2) 1990 e_1_2_6_8_2 e_1_2_6_18_2 e_1_2_6_9_2 e_1_2_6_19_2 Broekemeier KM (e_1_2_6_4_2) 1989; 264 e_1_2_6_6_2 e_1_2_6_5_2 e_1_2_6_12_2 e_1_2_6_13_2 e_1_2_6_2_2 e_1_2_6_10_2 e_1_2_6_11_2 e_1_2_6_16_2 e_1_2_6_17_2 e_1_2_6_14_2 e_1_2_6_15_2 |
| References_xml | – reference: Kristal BS, Matsuda M, Yu BP. Abnormalities in the mitochondrial permeability transition in diabetic rats. Biochem Biophys Res Commun 1996; 222: 519-523. – reference: Bernardi P, Colonna R, Costantini P, et al. The mitochondrial permeability transition. Biofactors 1998; 8: 273-281. – reference: Santos MS, Santos DL, Palmeira CM, Seica R, Moreno AJ, Oliveira CR. Brain and liver mitochondria isolated from diabetic Goto-Kakizaki rats show different susceptibility to induced oxidative stress. Diabetes Metab Res Rev 2001; 17(3): 223-230. – reference: Kamo N, Muratsugu M, Hongoh R, Kobatake Y. Membrane potential of mitochondria measured with an electrode sensitive to tetraphenyl phosphonium and relationship between proton electrochemical potential and phosphorylation potential in steady state. J Membr Biol 1979; 49: 105-121. – reference: Kowaltowski AJ, Castilho RF, Vercesi AE. Mitochondrial permeability transition and oxidative stress. FEBS Lett 2001; 495: 12-15. – reference: Crompton M. The mitochondrial permeability transition pore and its role in cell death. Biochem J 1999; 341: 233-249. – reference: Rajdev S, Reynolds IJ. Calcium Green-5N, a novel fluorescent probe for monitoring high intracellular free Ca2+ concentrations associated with glutamate excitotoxicity in cultured rat brain neurons. Neurosci Lett 1993; 162: 149-152. – reference: Santos DL, Palmeira CM, Seica R, et al. Diabetes and mitochondrial oxidative stress: a study using heart mitochondria from the diabetic Goto-Kakizaki rat. Mol Cell Biochem 2003; 246(1-2): 163-170. – reference: Oliveira PJ, Rolo AP, Seiça R, Palmeira CP, Santos MS, Moreno AJ. Decreased susceptibility of heart mitochondria from diabetic GK rats to mitochondrial permeability transition induced by calcium/phosphate. Biosci Rep 2001; 21: 55-62. – reference: Santos MS, Duarte AI, Matos MJ, Proenca T, Seica R, Oliveira CR. Synaptosomes isolated from Goto-Kakizaki diabetic rat brain exhibit increased resistance to oxidative stress: role of vitamin E. Life Sci 2000; 67(25): 3061-3073. – reference: Lass A, Kwong L, Sohal RS. Mitochondrial coenzyme Q content and aging. Biofactors 1999; 9: 199-205. – reference: Takayanagi R, Takeshige T, Minakami P. NADH- and NADPH-dependent lipid peroxidation in bovine submitochondrial particles. Biochem J 1980; 192: 853-860. – reference: Broekemeier KM, Dempsey ME, Pfeiffer DR. Cyclosporin A Is a Potent Inhibitor of the inner membrane mitochondrial transition in liver mitochondria. J Biol Chem 1989; 264: 7826-7830. – reference: Flatt P, Abdel-Wahab Y, Boyd AC. Pancreatic B-cell dysfunction and glucose toxicity in non-insulin-dependent diabetes. Proc Nutr Soc 1997; 56: 243-262. – reference: Rizzuto R, Pinton P, Brini M, Chiesa A, Filippin L, Pozzan T. Mitochondria as biosensors of calcium microdomains. Cell Calcium 1999; 26: 193-199. – reference: Takada M, Ikenoya S, Yuzuriha T, Katayama K. Simultaneous determination of reduced and oxidized ubiquinones. 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Renal disease associated with diabetes mellitus is a major problem among diabetic patients. The role of mitochondria in the pathogenesis of diabetes... Renal disease associated with diabetes mellitus is a major problem among diabetic patients. The role of mitochondria in the pathogenesis of diabetes has... Background Renal disease associated with diabetes mellitus is a major problem among diabetic patients. The role of mitochondria in the pathogenesis of diabetes... |
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| SubjectTerms | Analysis of Variance Animals Biological and medical sciences Calcium - metabolism Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - metabolism Diabetes. Impaired glucose tolerance Diabetic Nephropathies - complications Diabetic Nephropathies - metabolism Disease Models, Animal Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Goto-Kakizaki rat Intracellular Membranes - metabolism Kidney Diseases - etiology Kidney Diseases - metabolism kidney mitochondria Male Medical sciences Membrane Potentials - physiology Mitochondria - metabolism mitochondrial permeability transition Permeability Rats Rats, Inbred Strains Rats, Wistar Reference Values type 2 diabetes Ubiquinone - metabolism Vitamin E - metabolism |
| Title | Calcium-dependent mitochondrial permeability transition is augmented in the kidney of Goto-Kakizaki diabetic rat |
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