Ascorbate-Dependent Enhancement of Nitric Oxide Formation in Activated Macrophages

Mizutani, Akifumi; Maki, Hideki; Torii, Yasuyoshi; Hitomi, Kiyotaka; Tsukagoshi, Norihiro

doi:10.1006/niox.1998.0182

Cited by 32 publications

(17 citation statements)

References 19 publications

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“…In vitro studies have shown that vitamin C selectively influences cytokine production. 105 Ascorbate increases inducible nitric oxide synthetase production by macrophages activated by LPS 106 and also regulates the phagocytic process by decreasing free radical production and thus potentially reduces the severity of the endotoxin response. 107 Interesting new studies show that during stress exercise, contracting skeletal muscle is a major contributor to the exercise-induced increase of plasma IL-6 and that supplementation with vitamins C and E attenuates this response.…”

Section: Antioxidant Vitamin Deficiencymentioning

confidence: 99%

Mechanisms of nutrient modulation of the immune response

Cunningham‐Rundles

McNeeley

Moon

2005

Journal of Allergy and Clinical Immunology

451

330

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Section: Antioxidant Vitamin Deficiencymentioning

confidence: 99%

Mechanisms of nutrient modulation of the immune response

Cunningham‐Rundles

McNeeley

Moon

2005

Journal of Allergy and Clinical Immunology

451

330

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“…46 It has also been shown that vitamin C increases eNOS gene expression. 46,47 There are several data that support the inhibitory effect of antioxidants on inflammation and indirectly suggest the role of ROS as an activator of the inflammatory response. ␣-Tocopherol helps decrease the influx of leukocytes in the vasculature by downregulating the expression of E-selectin, decreasing interleukin-1 secretion from monocytes, and attenuating the activation of NF-B.…”

Section: Pharmacological Perspectivesmentioning

confidence: 99%

Heart Failure, Redox Alterations, and Endothelial Dysfunction

2001

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Abstract-Heart failure is characterized by neurohumoral alterations, such as activation of the sympathetic nervous system, stimulation of the renin-angiotensin system, increased activity of the endothelin system, increased production of norepinephrine, and increased circulating levels of cytokines. Oxidative stress is associated with the formation of reactive oxygen species (ROS). The myocardium has enzymes that stimulate ROS generation and enzymes with antioxidant effects. Several studies have suggested that ROS are increased in the failing heart. ROS may contribute to the pathophysiology of heart failure by initiating myocyte apoptosis and exerting direct negatively inotropic effects through the reduction of cytosolic intracellular free calcium. However, mechanisms such as endothelial dysfunction and inflammation have also been involved in the progression of heart failure. Antioxidants (eg, vitamin C) seem to improve endothelial functionality and reduce the inflammatory response in patients with heart failure. Therefore, in this review, we analyzed the involvement of ROS in the cellular and molecular mechanisms associated with endothelial dysfunction in heart failure.

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“…NO may lose an electron to form nitrosonium cation (NO + ), which can combine with the superoxide radicals to form peroxynitrite (ONOO -), a highly active free radical with fierce cytotoxicity [5] . In pathological conditions, significant activation of iNOS by the release of inflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), can increase NO concentration [6] . It was reported that endog enous NO is involved in for mation of pancreatic edema in L-arginine-induced acute pancreatitis by increasing the vascular per meability and protein extravasation [7] .…”

Section: Discussionmentioning

confidence: 99%

Protective effect of inducible nitric oxide synthase inhibitor on pancreas transplantation in rats

Bai-Feng¹,

Li²,

Yongfeng³

et al. 2007

WJG

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AIM:To investigate the effect of inducible nitric oxide synthase inhibitor, aminoguanidine, on pancreas transplantation in rats. METHODS:A model of pancreas transplantation was established in rats. Streptozotocin-induced diabetic male Wistar rats were randomly assigned to sham-operation control group (n = 6), transplant control group (n = 6), and aminoguanidine (AG) treatment group (n = 18). In the AG group, aminoguanidine was added to intravascular infusion as the onset of reperfusion at the dose of 60 mg/kg, 80 mg/kg, 100 mg/kg body weight, respectively. Serum nitric oxide (NO) level, blood sugar and amylase activity were detected. Nitric oxide synthase (NOS) test kit was used to detect the pancreas cNOS and inducible NOS (iNOS) activity. Pancreas sections stained with HE and immunohistochemistry were evaluated under a light microscope. RESULTS:As compared with the transplant control group, the serum NO level and amylase activity decreased obviously and the evidence for pancreas injury was much less in the AG group. The AG (80 mg/kg body weight) group showed the most significant difference in NO and amylase (NO: 66.0 ± 16.6 vs 192.3 ± 60.0, P < 0.01 and amylase: 1426 ± 177 vs 4477 ± 630, P < 0.01).The expression and activity of tissue iNOS, and blood sugar in the AG (80 mg/kg body weight) group were much lower than those in the transplant control group (iNOS: 2.01 ± 0.23 vs 26.59 ± 5.78, P < 0.01 and blood sugar: 14.2 ± 0.9 vs 16.8 ± 1.1, P < 0.01). CONCLUSION:Selective iNOS inhibitor, aminoguanidine as a free radical, has a protective effect on pancreas transplantation in rats by inhibiting NO and reducing its toxicity.

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Ascorbate-Dependent Enhancement of Nitric Oxide Formation in Activated Macrophages

Cited by 32 publications

References 19 publications

Mechanisms of nutrient modulation of the immune response

Mechanisms of nutrient modulation of the immune response

Heart Failure, Redox Alterations, and Endothelial Dysfunction

Protective effect of inducible nitric oxide synthase inhibitor on pancreas transplantation in rats

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