Interactions of water soluble porphyrins with Z-poly(dG-dC)

Pasternack, Robert F.; Sidney, David; Hunt, Peter; Snowden, Elizabeth A.; Gibbs, Julian H.

doi:10.1093/nar/14.9.3927

Cited by 26 publications

(10 citation statements)

References 27 publications

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“…The role of hydrogen peroxide was confirmed by the experiments with MnTMPyP, since this SOD/catalase mimetic (Pasternack et al, 1986) nearly abolished the response. Ferrous ions catalyse interactions between hydrogen peroxide and superoxide anions, producing hydroxyl radicals.…”

Section: Discussionmentioning

confidence: 71%

Oxygen‐derived free radicals mediate endothelium‐dependent contractions in femoral arteries of rats with streptozotocin‐induced diabetes

Shi

Man

et al. 2007

British J Pharmacology

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Background and purpose:The present experiments were designed to study the contribution of oxygen-derived free radicals to endothelium-dependent contractions in femoral arteries of rats with streptozotocin-induced diabetes. Experimental approach: Rings with and without endothelium were suspended in organ chambers for isometric tension recording. The production of oxygen-derived free radicals in the endothelium was measured with 2 0 ,7 0 -dichlorodihydrofluorescein diacetate using confocal microscopy. The presence of protein was measured by western blotting. Key results: In the presence of L-NAME, the calcium ionophore A23187 induced larger endothelium-dependent contractions in femoral arteries from diabetic rats. Tiron, catalase, deferoxamine and MnTMPyP, but not superoxide dismutase reduced the response, suggesting that oxygen-derived free radicals are involved in the endothelium-dependent contraction. In the presence of L-NAME, A23187 increased the fluorescence signal in femoral arteries from streptozotocin-treated, but not in those from control rats, confirming that the production of oxygen-derived free radicals contributes to the enhanced endotheliumdependent contractions in diabetes. Exogenous H 2 O 2 caused contractions in femoral arterial rings without endothelium which were reduced by deferoxamine, indicating that hydroxyl radicals contract vascular smooth muscle and thus could be an endothelium-derived contracting factor in diabetes. The reduced presence of Mn-SOD and the decreased activity of catalase in femoral arteries from streptozotocin-treated rats demonstrated the presence of a redox abnormality in arteries from rats with diabetes. Conclusions and implications: These findings suggest that the redox abnormality resulting from diabetes increases oxidative stress which facilitates and/or causes endothelium-dependent contractions.

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Section: Discussionmentioning

confidence: 71%

Oxygen‐derived free radicals mediate endothelium‐dependent contractions in femoral arteries of rats with streptozotocin‐induced diabetes

Shi

Man

et al. 2007

British J Pharmacology

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“…In the present experiments, apocynin did not affect either body weight or blood glucose, suggesting that this antioxidant does not interfere per se with the diabetic process. Moreover, MnTMPyP, a superoxide dismutase (SOD)/catalase mimetic ( Pasternack et al ., 1986 ), also normalized the response to TP activation in the femoral artery from STZ‐treated rats, supporting the involvement of oxygen‐derived free radicals in the hyper‐responsiveness observed in arteries from diabetic animals.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress and COX cause hyper‐responsiveness in vascular smooth muscle of the femoral artery from diabetic rats

Shi

Vanhoutte

2008

British J Pharmacology

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Background and purpose: To investigate the dysfunction of vascular smooth muscle in streptozotocin-induced diabetic rats. Experimental approach: Rings without endothelium of femoral arteries were suspended in organ chambers for isometric tension recording. The production of oxygen-derived free radicals was measured with 2 0 ,7 0 -dichlorodihydrofluorescein diacetate using confocal microscopy. The protein expressions were measured by western blotting. Key results: The concentration-response curves to U46619 and phenylephrine, but not that to KCl, were shifted to the left, suggesting a hypersensitivity of cell membrane receptors in diabetes. Exogenous oxygen-derived free radicals induced greater vasoconstrictions in the femoral artery from diabetic rats. Chronic treatment with apocynin (inhibitor of NADPH oxidase) and acute exposure to MnTMPyP (SOD/catalase mimetic) normalized the response. The catalase activity and the total glutathione level were reduced in arteries from streptozotocin-treated rats, confirming a redox abnormality. The basal oxidative state was higher in arteries from streptozotocin-treated rats and reduced in arteries from apocynin-and streptozotocin-treated rats, suggesting that the functional changes in diabetes are due to a chronic increase in oxidative stress. In the arteries of streptozotocin-treated rats, inhibitors of COX-1 and/or COX-2 prevented the hypersensitivity and reduced the increase in oxidative stress caused by phenylephrine and U46619, suggesting that both isoforms contribute to the smooth muscle dysfunction. The expression of proteins for COX-1 and COX-2 was increased in arteries of streptozotocin-treated rats and reduced in preparations of apocynin-and streptozotocin-treated rats. Conclusions and implications: Chronic diabetes and the resulting increased oxidative stress activate the production of COXderived vasoconstrictor prostanoids causing hypersensitivity of vascular smooth muscle.

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“…[20,21] However, few studies have been performed on the interactions of cationic porphyrins with Z-DNA because the intercalation of porphyrins reverts the helix back to the B form. [23] The latter data suggest that pentacoordinated cationic metalloporphyrins, such as the zinc(ii) derivative of meso-tetrakis(4-N-methylpyridyl)porphyrin (ZnT4, 1; Figure 1), should be an ideal chiroptical probe for Z-DNA because the axially coordinated water molecule hinders intercalation [24][25][26][27][28] and prevents the Z-to-B transition.…”

mentioning

confidence: 99%