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Correlations between Endothelial Functions and ROS Detection in Diabetic Microvascular Wall: Early and Late Ascorbic Acid Supplementation.

Sridulyakul P, Wongeak-In N, Patumraj S - Int J Vasc Med (2012)

Bottom Line: On 12th week after STZ injection, the findings showed that in DM group, Ach (10(-5) M)-induced vasodilatation was decreased, while the number of leukocyte adhesion was increased significantly (P < 0.01).By using dihydrorhodamine 123, our findings also indicated that the existing of ROS productions on diabetic arteriolar and venular walls were different significantly (ROS(arteriole) = 165.89 ± 24.59 and ROS(venule) = 172.26 ± 34.70) (P < 0.05).Moreover by using BH4 inhibitor to induce increase in arteriolar ROS, the results also confirmed that AA could improve endothelial function with closed correlation to its potential to reduce vascular ROS content.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Faculty of Science, Srinakharinwirot University, Bangkok 10110, Thailand.

ABSTRACT
The correlation between endothelial function and reactive oxygen species detecting from diabetic microvascular wall and the antioxidant effect of ascorbic acid (AA) during early and late phases of diabetic induction were determined. Male Spraque-Dawley rats were divided into four groups: control, diabetes rats (DM, using iv.injection of 55 mg/kg BW streptozotocin, (STZ)), and two groups of DM rats treated with AA (1 g/L, (STZ)) starting on day 2 (DM + AAday2) and week 6th (DM + AA6wk). On 12th week after STZ injection, the findings showed that in DM group, Ach (10(-5) M)-induced vasodilatation was decreased, while the number of leukocyte adhesion was increased significantly (P < 0.01). Interestingly, these abnormalities induced by DM could be protected or improved in both AA-treated groups, DM + AAday2 and DM + AA6wk. By using dihydrorhodamine 123, our findings also indicated that the existing of ROS productions on diabetic arteriolar and venular walls were different significantly (ROS(arteriole) = 165.89 ± 24.59 and ROS(venule) = 172.26 ± 34.70) (P < 0.05). Moreover by using BH4 inhibitor to induce increase in arteriolar ROS, the results also confirmed that AA could improve endothelial function with closed correlation to its potential to reduce vascular ROS content.

No MeSH data available.


Related in: MedlinePlus

The diagram represents the proposed mechanism of ascorbic acid (AA) in attenuating reactive oxygen species (ROS) production when DAHP inhibited BH4 and caused eNOS uncoupling. Similar to diabetic-induced endothelial cells dysfunction in associated with BH4 deficiency.
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fig6: The diagram represents the proposed mechanism of ascorbic acid (AA) in attenuating reactive oxygen species (ROS) production when DAHP inhibited BH4 and caused eNOS uncoupling. Similar to diabetic-induced endothelial cells dysfunction in associated with BH4 deficiency.

Mentions: At this point, it may be suggested that in the situation of DAHP-induced BH4 deficiency, eNOS uncoupling is produced as it will generate O2− and consequently convert to H2O2− as demonstrated by DHR-123 detection. In addition when eNOS uncoupling, less of NO is produced, therefore, the Ach-induced vasodilatation becomes significantly decreased in CON + DAHP group. In Figure 6, this idea is summarized and presented for supporting the beneficial mechanism of vitamin C on protecting endothelial function against oxidative stress condition.


Correlations between Endothelial Functions and ROS Detection in Diabetic Microvascular Wall: Early and Late Ascorbic Acid Supplementation.

Sridulyakul P, Wongeak-In N, Patumraj S - Int J Vasc Med (2012)

The diagram represents the proposed mechanism of ascorbic acid (AA) in attenuating reactive oxygen species (ROS) production when DAHP inhibited BH4 and caused eNOS uncoupling. Similar to diabetic-induced endothelial cells dysfunction in associated with BH4 deficiency.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3368388&req=5

fig6: The diagram represents the proposed mechanism of ascorbic acid (AA) in attenuating reactive oxygen species (ROS) production when DAHP inhibited BH4 and caused eNOS uncoupling. Similar to diabetic-induced endothelial cells dysfunction in associated with BH4 deficiency.
Mentions: At this point, it may be suggested that in the situation of DAHP-induced BH4 deficiency, eNOS uncoupling is produced as it will generate O2− and consequently convert to H2O2− as demonstrated by DHR-123 detection. In addition when eNOS uncoupling, less of NO is produced, therefore, the Ach-induced vasodilatation becomes significantly decreased in CON + DAHP group. In Figure 6, this idea is summarized and presented for supporting the beneficial mechanism of vitamin C on protecting endothelial function against oxidative stress condition.

Bottom Line: On 12th week after STZ injection, the findings showed that in DM group, Ach (10(-5) M)-induced vasodilatation was decreased, while the number of leukocyte adhesion was increased significantly (P < 0.01).By using dihydrorhodamine 123, our findings also indicated that the existing of ROS productions on diabetic arteriolar and venular walls were different significantly (ROS(arteriole) = 165.89 ± 24.59 and ROS(venule) = 172.26 ± 34.70) (P < 0.05).Moreover by using BH4 inhibitor to induce increase in arteriolar ROS, the results also confirmed that AA could improve endothelial function with closed correlation to its potential to reduce vascular ROS content.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Faculty of Science, Srinakharinwirot University, Bangkok 10110, Thailand.

ABSTRACT
The correlation between endothelial function and reactive oxygen species detecting from diabetic microvascular wall and the antioxidant effect of ascorbic acid (AA) during early and late phases of diabetic induction were determined. Male Spraque-Dawley rats were divided into four groups: control, diabetes rats (DM, using iv.injection of 55 mg/kg BW streptozotocin, (STZ)), and two groups of DM rats treated with AA (1 g/L, (STZ)) starting on day 2 (DM + AAday2) and week 6th (DM + AA6wk). On 12th week after STZ injection, the findings showed that in DM group, Ach (10(-5) M)-induced vasodilatation was decreased, while the number of leukocyte adhesion was increased significantly (P < 0.01). Interestingly, these abnormalities induced by DM could be protected or improved in both AA-treated groups, DM + AAday2 and DM + AA6wk. By using dihydrorhodamine 123, our findings also indicated that the existing of ROS productions on diabetic arteriolar and venular walls were different significantly (ROS(arteriole) = 165.89 ± 24.59 and ROS(venule) = 172.26 ± 34.70) (P < 0.05). Moreover by using BH4 inhibitor to induce increase in arteriolar ROS, the results also confirmed that AA could improve endothelial function with closed correlation to its potential to reduce vascular ROS content.

No MeSH data available.


Related in: MedlinePlus