PubMed · 13968986
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G F BAHR. Acridine-orange fluorescence method.. https://pubmed.ncbi.nlm.nih.gov/13968986/
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Using clonogenic survival assays, we demonstrated that a new platinum-acridine hybrid agent, PT-ACRAMTU, is cytotoxic in SNB19 and U87MG glioblastoma cells at low-micromolar concentrations. PT-ACRAMTU is more cytotoxic than ACRAMTU (the platinum-free acridine), acts in a time and dose dependent manner, and appears to generate an apoptotic response in both cell lines on the basis of increased caspase-3 activity.
Dehydrogenation of 10-methyl-9,10-dihydroacridine (AcrH(2)) by dioxygen (O(2)) proceeds efficiently, accompanied by the two-electron and four-electron reduction of O(2) to produce H(2)O(2) and H(2)O, which are effectively catalyzed by monomeric cobalt porphyrins and cofacial dicobalt porphyrins in the presence of perchloric acid (HClO(4)) in acetonitrile (MeCN) and benzonitrile (PhCN), respectively. The cobalt porphyrin catalyzed two-electron reduction of O(2) also occurs efficiently by 9-alkyl-10-methyl-9,10-dihydroacridines (AcrHR; R = Me, Et, and CH(2)COOEt) to yield 9-alkyl-10-methylacridinium ion (AcrR+) and H(2)O(2). In the case of R = Bu(t) and CMe(2)COOMe, however, the catalytic two-electron and four-electron reduction of O(2) by AcrHR results in oxygenation of the alkyl group of AcrHR rather than dehydrogenation to yield 10-methylacridinium ion (AcrH+) and the oxygenated products of the alkyl groups, i.e., the corresponding hydroperoxides (ROOH) and the alcohol (ROH), respectively. The catalytic mechanisms of the dehydrogenation vs the oxygenation of AcrHR in the two-electron and four-electron reduction of O(2), catalyzed by monomeric cobalt porphyrins and cofacial dicobalt porphyrins, respectively, are discussed in relation to the C(9)-H or C(9)-C bond cleavage of AcrHR radical cations produced in the electron-transfer oxidation of AcrHR.
The roles of nitric oxide (NO) and plasma renin activity (PRA) in the depressor response to chronic administration of Tempol in spontaneously hypertensive rats (SHR) are not clear. The present study was done to determine the effect of 2 wk of Tempol treatment on blood pressure [mean arterial pressure (MAP)], oxidative stress, and PRA in the presence or absence of chronic NO synthase inhibition. SHR were divided into four groups: control, Tempol (1 mmol/l) alone, nitro-L-arginine methyl ester (L-NAME, 4.5 mg x g(-1).day(-1)) alone, and Tempol + L-NAME or 2 wk. With Tempol, MAP decreased by 22%: 191 +/- 3 and 162 +/- 21 mmHg for control and Tempol, respectively (P < 0.05). L-NAME increased MAP by 16% (222 +/- 2 mmHg, P < 0.01), and L-NAME + Tempol abolished the depressor response to Tempol (215 +/- 3 mmHg, P < 0.01). PRA was not affected by Tempol but was increased slightly with L-NAME alone and 4.4-fold with L-NAME + Tempol. Urinary nitrate/nitrite increased with Tempol and decreased with L-NAME and L-NAME + Tempol. Tempol significantly reduced oxidative stress in the presence and absence of L-NAME. In conclusion, in SHR, Tempol administration for 2 wk reduces oxidative stress in the presence or absence of NO, but in the absence of NO, Tempol is unable to reduce MAP. Therefore, NO, but not changes in PRA, plays a major role in the blood pressure-lowering effects of Tempol. These data suggest that, in hypertensive individuals with endothelial damage and chronic NO deficiency, antioxidants may be able to reduce oxidative stress but not blood pressure.