Vol 47: Lipoic acid, but not tempol, preserves vascular compliance and decreases medial calcification in a model of elastocalcinosis.Report as inadecuate



 Vol 47: Lipoic acid, but not tempol, preserves vascular compliance and decreases medial calcification in a model of elastocalcinosis.


Vol 47: Lipoic acid, but not tempol, preserves vascular compliance and decreases medial calcification in a model of elastocalcinosis. - Download this document for free, or read online. Document in PDF available to download.

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This article is from Brazilian Journal of Medical and Biological Research, volume 47.AbstractVascular calcification decreases compliance and increases morbidity. Mechanisms of this process are unclear. The role of oxidative stress and effects of antioxidants have been poorly explored. We investigated effects of the antioxidants lipoic acid LA and tempol in a model of atherosclerosis associated with elastocalcinosis. Male New Zealand white rabbits 2.5-3.0 kg were fed regular chow controls or a 0.5% cholesterol chol diet+104 IU-day vitamin D2 vitD for 12 weeks, and assigned to treatment with water vehicle, n=20, 0.12 mmol·kg-1·day-1 LA n=11 or 0.1 mmol·kg-1·day-1 tempol n=15. Chol+vitD-fed rabbits developed atherosclerotic plaques associated with expansive remodeling, elastic fiber disruption, medial calcification, and increased aortic stiffness. Histologically, LA prevented medial calcification by ∼60% and aortic stiffening by ∼60%. LA also preserved responsiveness to constrictor agents, while intima-media thickening was increased. In contrast to LA, tempol was associated with increased plaque collagen content, medial calcification and aortic stiffness, and produced differential changes in vasoactive responses in the chol+vitD group. Both LA and tempol prevented superoxide signals with chol+vitD. However, only LA prevented hydrogen peroxide-related signals with chol+vitD, while tempol enhanced them. These data suggest that LA, opposite to tempol, can minimize calcification and compliance loss in elastocalcionosis by inhibition of hydrogen peroxide generation.



Author: Bassi, E.; Liberman, M.; Martinatti, M.K.; Bortolotto, L.A.; Laurindo, F.R.M.

Source: https://archive.org/







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