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Impaired mitochondrial respiratory functions and oxidative stress in streptozotocin-induced diabetic rats.

Raza H, Prabu SK, John A, Avadhani NG - Int J Mol Sci (2011)

Bottom Line: These animals showed a persistent increase in reactive oxygen and nitrogen species (ROS and RNS, respectively) production.Mitochondrial matrix aconitase, a ROS sensitive enzyme, was markedly inhibited in the diabetic rat tissues.Increased expression of oxidative stress marker proteins Hsp-70 and HO-1 was also observed along with increased expression of nitric oxide synthase.

View Article: PubMed Central - PubMed

ABSTRACT
We have previously shown a tissue-specific increase in oxidative stress in the early stages of streptozotocin (STZ)-induced diabetic rats. In this study, we investigated oxidative stress-related long-term complications and mitochondrial dysfunctions in the different tissues of STZ-induced diabetic rats (>15 mM blood glucose for 8 weeks). These animals showed a persistent increase in reactive oxygen and nitrogen species (ROS and RNS, respectively) production. Oxidative protein carbonylation was also increased with the maximum effect observed in the pancreas of diabetic rats. The activities of mitochondrial respiratory enzymes ubiquinol: cytochrome c oxidoreductase (Complex III) and cytochrome c oxidase (Complex IV) were significantly decreased while that of NADH:ubiquinone oxidoreductase (Complex I) and succinate:ubiquinone oxidoreductase (Complex II) were moderately increased in diabetic rats, which was confirmed by the increased expression of the 70 kDa Complex II sub-unit. Mitochondrial matrix aconitase, a ROS sensitive enzyme, was markedly inhibited in the diabetic rat tissues. Increased expression of oxidative stress marker proteins Hsp-70 and HO-1 was also observed along with increased expression of nitric oxide synthase. These results suggest that mitochondrial respiratory complexes may play a critical role in ROS/RNS homeostasis and oxidative stress related changes in type 1 diabetes and may have implications in the etiology of diabetes and its complications.

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Activities of respiratory complexes in STZ-induced diabetes. Mitochondrial protein (10–25 μg) from pancreas, liver, kidney and brain of control and diabetic rats were used for the assays of respiratory chain enzyme complexes as described in the Materials and Methods. (a) Complex I, NADH: ubiquinone oxidoreductase activity; (b) Complex II, succinate:ubiquinone oxidoreductase activity; (c) Complex III, ubiquinol: ferrocytochrome c oxidoreductase activity; and (d) Complex IV, cytochrome c oxidase activity. The values are mean ± S.E.M for three determinations. * indicate significant difference (P < 0.05) from the controls. (□) Control; (▪) Diabetic.
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f4-ijms-12-03133: Activities of respiratory complexes in STZ-induced diabetes. Mitochondrial protein (10–25 μg) from pancreas, liver, kidney and brain of control and diabetic rats were used for the assays of respiratory chain enzyme complexes as described in the Materials and Methods. (a) Complex I, NADH: ubiquinone oxidoreductase activity; (b) Complex II, succinate:ubiquinone oxidoreductase activity; (c) Complex III, ubiquinol: ferrocytochrome c oxidoreductase activity; and (d) Complex IV, cytochrome c oxidase activity. The values are mean ± S.E.M for three determinations. * indicate significant difference (P < 0.05) from the controls. (□) Control; (▪) Diabetic.

Mentions: Figure 4 shows alterations in the activities of mitochondrial respiratory complexes. On a comparative basis, kidney and liver showed the highest activities for all the four complexes studied. Complex I and II activities in the tissues from diabetic rats were moderately increased (20–30% from control; P < 0.05). Brain, however, showed no increase in Complex II activity. The activities of Complex III and IV from diabetic rats were, however, significantly decreased (25–36%; P < 0.05) in pancreas, liver and kidney. Brain, however, showed no significant inhibition (7–10%; P > 0.05) in these activities.


Impaired mitochondrial respiratory functions and oxidative stress in streptozotocin-induced diabetic rats.

Raza H, Prabu SK, John A, Avadhani NG - Int J Mol Sci (2011)

Activities of respiratory complexes in STZ-induced diabetes. Mitochondrial protein (10–25 μg) from pancreas, liver, kidney and brain of control and diabetic rats were used for the assays of respiratory chain enzyme complexes as described in the Materials and Methods. (a) Complex I, NADH: ubiquinone oxidoreductase activity; (b) Complex II, succinate:ubiquinone oxidoreductase activity; (c) Complex III, ubiquinol: ferrocytochrome c oxidoreductase activity; and (d) Complex IV, cytochrome c oxidase activity. The values are mean ± S.E.M for three determinations. * indicate significant difference (P < 0.05) from the controls. (□) Control; (▪) Diabetic.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3116180&req=5

f4-ijms-12-03133: Activities of respiratory complexes in STZ-induced diabetes. Mitochondrial protein (10–25 μg) from pancreas, liver, kidney and brain of control and diabetic rats were used for the assays of respiratory chain enzyme complexes as described in the Materials and Methods. (a) Complex I, NADH: ubiquinone oxidoreductase activity; (b) Complex II, succinate:ubiquinone oxidoreductase activity; (c) Complex III, ubiquinol: ferrocytochrome c oxidoreductase activity; and (d) Complex IV, cytochrome c oxidase activity. The values are mean ± S.E.M for three determinations. * indicate significant difference (P < 0.05) from the controls. (□) Control; (▪) Diabetic.
Mentions: Figure 4 shows alterations in the activities of mitochondrial respiratory complexes. On a comparative basis, kidney and liver showed the highest activities for all the four complexes studied. Complex I and II activities in the tissues from diabetic rats were moderately increased (20–30% from control; P < 0.05). Brain, however, showed no increase in Complex II activity. The activities of Complex III and IV from diabetic rats were, however, significantly decreased (25–36%; P < 0.05) in pancreas, liver and kidney. Brain, however, showed no significant inhibition (7–10%; P > 0.05) in these activities.

Bottom Line: These animals showed a persistent increase in reactive oxygen and nitrogen species (ROS and RNS, respectively) production.Mitochondrial matrix aconitase, a ROS sensitive enzyme, was markedly inhibited in the diabetic rat tissues.Increased expression of oxidative stress marker proteins Hsp-70 and HO-1 was also observed along with increased expression of nitric oxide synthase.

View Article: PubMed Central - PubMed

ABSTRACT
We have previously shown a tissue-specific increase in oxidative stress in the early stages of streptozotocin (STZ)-induced diabetic rats. In this study, we investigated oxidative stress-related long-term complications and mitochondrial dysfunctions in the different tissues of STZ-induced diabetic rats (>15 mM blood glucose for 8 weeks). These animals showed a persistent increase in reactive oxygen and nitrogen species (ROS and RNS, respectively) production. Oxidative protein carbonylation was also increased with the maximum effect observed in the pancreas of diabetic rats. The activities of mitochondrial respiratory enzymes ubiquinol: cytochrome c oxidoreductase (Complex III) and cytochrome c oxidase (Complex IV) were significantly decreased while that of NADH:ubiquinone oxidoreductase (Complex I) and succinate:ubiquinone oxidoreductase (Complex II) were moderately increased in diabetic rats, which was confirmed by the increased expression of the 70 kDa Complex II sub-unit. Mitochondrial matrix aconitase, a ROS sensitive enzyme, was markedly inhibited in the diabetic rat tissues. Increased expression of oxidative stress marker proteins Hsp-70 and HO-1 was also observed along with increased expression of nitric oxide synthase. These results suggest that mitochondrial respiratory complexes may play a critical role in ROS/RNS homeostasis and oxidative stress related changes in type 1 diabetes and may have implications in the etiology of diabetes and its complications.

Show MeSH
Related in: MedlinePlus