Evaluation of free radical scavengers in studies of lymphocyte-mediated cytolysis

Devlin, Richard G.; Lin, C. Shirley; Perper, R. J.; Dougherty, Harry W.

doi:10.1016/0162-3109(81)90016-3

Cited by 36 publications

(9 citation statements)

References 39 publications

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“…The non-enzymatic scavenger tiron almost inhibited the CL signal in response to intact coronary arteries, whereas the addition of SOD only partially inhibited the CL signal by about 50%. This difference may be explained by the fact that the macromolecule SOD is not able to penetrate cell membranes (Beckman, Minor, White, Repine, Rosen & Freeman, 1988), whereas small molecules like lucigenin (Paky, Michael, Burke-Wolin, Wolin & Gurtner, 1993) or tiron (Devlin, Lin, Perper & Dougherty, 1981) are. The observation that DPI significantly reduced the vascular generation of 2-suggests that a flavoprotein is involved.…”

Section: Discussionmentioning

confidence: 99%

Endothelial‐derived superoxide anions in pig coronary arteries: evidence from lucigenin chemiluminescence and histochemical techniques.

Brandes

Barton

Philippens

et al. 1997

The Journal of Physiology

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1. The generation of superoxide anions (02-) by intact pig coronary artery rings was measured using a lucigenin-enhanced chemiluminescence technique and a histochemical technique with Nitroblue Tetrazolium (NBT) staining. 2. Isolated arteries with intact endothelium generated 02 at a rate of 9 0 + 0-8 pmol min' (mg dry weight)-1; this rate was diminished by about 24% when the endothelium was removed. The NBT staining of arterial ring preparations showed formazan precipitation mainly in the intima. Arterial rings were pretreated with diethylthiocarbamate in order to inhibit Cu-Zn superoxide dismutase (SOD) activity which increased the 2-generation by 184 + 55% (n = 10; P < 0-01). Stimulation of protein kinase C with phorbol 12-myristate 13-acetate (5 FM) enhanced endothelium-dependent 2-generation by 136 + 20% (n = 19; P< 0-01). Neither stimulation with bradykinin or substance P, nor inhibition with NG-nitro-L-arginine methyl ester of endothelial nitric oxide synthase had a significant effect on 02-generation. In contrast, the inhibition of flavoproteins with diphenyliodonium 4. The results suggest that intact coronary arteries do generate O2-under basal conditions and that the endothelial layer significantly contributes to this phenomenon. This generation of 02-is greatly influenced by intrinsic SOD activity. It is suggested that basal vascular 02-generation is mainly due to membrane-bound NAD(P)H oxidase activity and/or tetrahydrobiopterin-dependent processes.

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Section: Discussionmentioning

confidence: 99%

Endothelial‐derived superoxide anions in pig coronary arteries: evidence from lucigenin chemiluminescence and histochemical techniques.

Brandes

Barton

Philippens

et al. 1997

The Journal of Physiology

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“…Bosentan (Veniant et al, 1994), a blocker of endothelin receptors did not prevent the further contraction, suggesting that it cannot be attributed to the release of enothelin-1. The observation that the TP-receptor blocker S18886 and superoxide dismutase plus tiron (Devlin et al, 1981) did not prevent it either, ruled out free radical-derived isoprostanes. Likewise, sulfaphenazole, an inhibitor of P450 monooxygenase (Veronese et al, 1990), did not inhibit the response, suggesting that it was not caused by P450 metabolites of arachidonic acid.…”

Section: Discussionmentioning

confidence: 99%

Augmented Endothelium-Derived Hyperpolarizing Factor-Mediated Relaxations Attenuate Endothelial Dysfunction in Femoral and Mesenteric, but Not in Carotid Arteries from Type I Diabetic Rats

Shi

Ku²,

Man³

et al. 2006

J Pharmacol Exp Ther

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Individual vascular beds exhibit differences in vascular reactivity. The present study investigates the effects of streptozotocininduced type I diabetes on endothelium-dependent responses of rat carotid, femoral, and mesenteric arteries. Rings with and without endothelium, suspended in organ chambers for isometric tension recording, were contracted with phenylephrine and exposed to increasing concentrations of acetylcholine. In carotid and femoral arteries, acetylcholine produced concentration-and endothelium-dependent relaxations that were abolished by N -nitro-L-arginine methyl ester (L-NAME; specific nitric-oxide synthase inhibitor) and were impaired slightly in preparations from streptozotocin-treated rats (STZ-rats). This impairment could be prevented by L-arginine. In femoral arteries incubated with L-NAME, acetylcholine caused endotheliumdependent contractions that were abolished by 3-[(6-amino-(4-chlorobenzensulfonyl)-2-methyl-5,6,7,8-tetrahydronapht]-1-yl) propionic acid (S18886) (antagonist of thromboxane A 2 /prostaglandins H 2 -receptors) and reversed to relaxation by indomethacin (inhibitor of cyclooxygenase). The latter relaxation was inhibited by charybdotoxin plus apamin, suggesting a role of endothelium-dependent hyperpolarizing factor (EDHF). This EDHF-mediated component was augmented slightly in arteries from STZ-rats. In mesenteric arteries, relaxations to acetylcholine were only partially inhibited by L-NAME, and the L-NAMEresistant component was abolished by charybdotoxin plus apamin. In the mesenteric arteries from STZ-rats, L-NAME-sensitive relaxations to acetylcholine were reduced and the EDHFcomponent was augmented. These findings demonstrate a marked heterogeneity in endothelium-dependent responses in rat arteries and their differential adaptation in the course of type I diabetes. In particular, the EDHF-mediated component not only compensates for the reduced bioavailability of nitric oxide in the femoral and mesenteric artery but also counteracts the augmented endothelium-dependent contractions in the former.The endothelial cells release both endothelium-derived relaxing factors and endothelium-derived contracting factors (EDCFs), which control the tone of the underlying smooth muscle. Endothelium-derived relaxing factors include NO, prostacyclin, and several endothelium-derived hyperpolarizing factors (EDHFs). Different vascular beds, exposed to varying local and neurohumoral influences, exhibit a marked heterogeneity in vascular responsiveness (Vanhoutte, 1978;Lü scher and Vanhoutte, 1990;Feletou and Vanhoutte, 2006). NO is a major contributor to endothelium-dependent relaxations in large conduit arteries, whereas endothelium-derived hyperpolarizing factor(s) play a predominant role in small arteries (Nagao et al., 1992;Shimokawa et al., 1996). Diabetes mellitus is characterized by hyperglycemia resulting from a defective secretion and/or action of insulin. Data on the impairment of endothelial function caused by type I diabetes are controversial. Thus, in blood vessels from...

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“…Background counts were determined from identically processed vessel-free incubations and subtracted from the readings obtained with vessels. Chemiluminescence was inhibited > 95% by pretreatment of arterial segments with 10 mM Tiron (4,5 dihydroxy-1,3-benzene sulfonic acid salt), a known scavenger of superoxide anions (36).…”

Section: Methodsmentioning

confidence: 99%

Dietary probucol preserves endothelial function in cholesterol-fed rabbits by limiting vascular oxidative stress and superoxide generation.

Keaney¹,

Xu²,

Cunningham³

et al. 1995

J. Clin. Invest.

197

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IntroductionExcess vascular oxidative stress and the local formation of oxidized LDL (ox-LDL) have been implicated in the development of impaired endothelium-dependent arterial relaxation in hypercholesterolemia and atherosclerosis. Dietary antioxidants limit LDL oxidation in vitro and treatment of cholesterol-fed rabbits with dietary antioxidants preserves endothelium-derived relaxing factor (EDRF) The vascular endothelium is important in the maintenance of vascular homeostasis. Normally, the vascular endothelium prevents inappropriate vasospasm and platelet adhesion to the vascular surface through the production of numerous paracrine factors (for review see reference 1). Principal among these mediators of vascular homeostasis is endothelium-derived relaxing factor (EDRF),' an endothelial product that has been identified as nitric oxide (NO) (2), or a closely related redoxactivated form of NO (3). This endothelial product relaxes vascular smooth muscle and prevents platelet adhesion to the endothelial surface through a cyclic 3 ',5 '-guanosine monophosphate-mediated mechanism (4, 5). Abnormalities in EDRF action have been described in association with known risk factors for acute vascular events including hypercholesterolemia (6) and atherosclerosis (7). These abnormalities develop early in the course of vascular disease (6,8) and may participate in the development of clinically significant vascular events.There are now several lines of evidence linking excess vascular oxidative stress to the impairment of EDRF action associated with hypercholesterolemia and atherosclerosis. Early in atherogenesis, LDL becomes entrapped in the subendothelial space of lesion-prone arterial sites where it is subject to oxidation by endothelial cells (9), smooth muscle cells (10), and resident monocyte/macrophages (11). Oxidized LDL (ox-LDL) inhibits receptor-mediated endothelium-dependent arterial relaxation (12) and signal transduction (13). Moreover, ox-LDL is cytotoxic (14)

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Evaluation of free radical scavengers in studies of lymphocyte-mediated cytolysis

Cited by 36 publications

References 39 publications

Endothelial‐derived superoxide anions in pig coronary arteries: evidence from lucigenin chemiluminescence and histochemical techniques.

Endothelial‐derived superoxide anions in pig coronary arteries: evidence from lucigenin chemiluminescence and histochemical techniques.

Augmented Endothelium-Derived Hyperpolarizing Factor-Mediated Relaxations Attenuate Endothelial Dysfunction in Femoral and Mesenteric, but Not in Carotid Arteries from Type I Diabetic Rats

Dietary probucol preserves endothelial function in cholesterol-fed rabbits by limiting vascular oxidative stress and superoxide generation.

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