Nitric oxide: basic science and clinical applications

Kam, P. C. A.; Govender, G.

doi:10.1111/j.1365-2044.1994.tb03525.x

Cited by 41 publications

(16 citation statements)

References 55 publications

(24 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Two of them, tumor necrosis factor and interleukin 1, are present in injured nerve, and secreted, at least in part, by macrophages (Nathan, 1987;Creange et al, 1997;Oka et al, 1998). In contrast to constitutive isoforms of NOS, which synthesize small quantities (picomoles) of NO, mediating messenger functions, iNOS synthesizes large quantities (nanomoles) of NO, extensively related with its cytotoxic effects in immune and inflammatory responses Moncada and Higgs, 1993;Kam and Govender, 1994;Schmidt and Walter, 1994;Kerwin et al, 1995). Mechanisms of NO cytotoxicity include DNA damage, by deamination and inhibition of ribonucleotide reductase (Kwon et al, 1991;Wink et al, 1991), and inhibition of mitochondrial enzymes (Stamler, 1994).…”

Section: Inosmentioning

confidence: 97%

Expression of three forms of nitric oxide synthase in peripheral nerve regeneration

González‐Hernández

Rustioni

1999

J. Neurosci. Res.

View full text Add to dashboard Cite

Nitric oxide (NO) is a short-lived molecule with messenger and cytotoxic functions in nervous, cardiovascular, and immune systems. Nitric oxide synthase (NOS), the enzyme responsible for NO synthesis, exists in three different forms: the neuronal (nNOS), present in discrete neuronal populations; the endothelial (eNOS), present in vascular endotheliun, and the inducible isoform (iNOS), expressed in various cell types when activated, including macrophages and glial cells. In this study, we have investigated the possible involvement of NO in Wallerian degeneration and the subsequent regeneration occurring after sciatic nerve ligature, using histochemistry and immunocytochemistry for the three NOS isoforms, at different postinjury periods. Two days after lesion, the three NOS isoforms are overexpressed, reaching their greatest expression during the second week. nNOS is upregulated in dorsal root ganglion neurons, centrifugally transported and accumulated in growing axons. eNOS is overexpressed in vasa nervorum of the distal stump and around ligature, and iNOS is induced in recruited macrophages. These findings indicate that different cellular sources contribute to maintain high levels of NO at the lesion site. The parallelism between NOS inductions and well-known repair phenomena suggests that NO, acting in different ways, may exert a beneficial effect on nerve regeneration.

show abstract

Section: Inosmentioning

confidence: 97%

Expression of three forms of nitric oxide synthase in peripheral nerve regeneration

González‐Hernández

Rustioni

1999

J. Neurosci. Res.

View full text Add to dashboard Cite

show abstract

“…In addition to its vasodilatatory action, many other biological activities of NO have been identified, including roles in neurotransmission, neural plasticity, cytotoxicity, inhibition of platelet aggregation, and modulation of inflammatory and immunological functions [see e.g., Moncada and Higgs, 1991;Kam and Govender, 1994;Salerno et al, 2002]. To date, three types of NO synthase (NOS), the family of enzymes catalyzing the formation of NO from arginine, have been identified and cloned.…”

Section: Expression Of Nitric Oxide Synthases Introductory Commentsmentioning

confidence: 99%

Effects of Ginkgo biloba extract (EGb 761) on gene expression: Possible relevance to neurological disorders and age‐associated cognitive impairment

DeFeudis¹

2002

Drug Development Research

View full text Add to dashboard Cite

Ginkgo biloba leaf extract (EGb 761), which contains many constituents, including flavonoid glycosides and terpenoids (ginkgolides, bilobalide), is used to treat cerebrovascular and peripheral vascular insufficiency, as well as cognitive impairment and other symptoms of dementia. Recent studies have indicated that these therapeutic effects of EGb 761 probably involve modification of the expression of many genes by actions involving several of its active constituents. As examples: EGb 761 and its ginkgolide B constituent inhibit the expression of the peripheral benzodiazepine receptor in the adrenal cortex and decrease circulating levels of corticosterone in the rat, effects that provide a mechanism for explaining the ''antistress'' action of the extract. Both the flavonoid and terpenoid constituents of EGb 761 decrease the expression of inducible nitric oxide synthase (iNOS), supporting an action of the extract of opposing the deleterious effects of excessive formation of NO. EGb 761 upregulates several genes that encode vital antioxidant enzymes, including heme oxygenase-1 and the regulatory and catalytic subunits of g-glutamyl-cysteinyl synthetase. Dietary treatment of mice with EGb 761 upregulates the expression of genes encoding neuronal tyrosine/threonine phosphatase 1 and microtubule-associated tau in the cerebral cortex, findings that are of interest since these proteins are associated with the intracellular neurofibrillary tangles found in the brain in Alzheimer's disease. Bilobalide upregulates two mitochondrial-DNA-encoded genes, subunit III of cytochrome c oxidase and subunit ND1 of NADH dehydrogenase, indicating a fundamental mechanism that may underlie EGb 761-induced neuroprotection. Collectively, such results indicate that the therapeutic effects of EGb 761 on cognitive impairment (dementia) may involve its action of altering gene expression. Drug Dev.

show abstract

“…The mechanism by which cisplatin exerts its cytotoxic response and organ toxicity is not fully understood, A growing body of evidence suggests that nitric oxide (NO'l, a free radical and a prominent vascular and neuronal messenger molecule responsible for endothelium-derived relaxing factor activity, may play at crucial role towards the development and/or exacerbation of various pathological conditions due to its altered metaholism (Trifiletti [992, Francis et aL 1993, Mascolo et ~d. 1993, Middleton et al 1993, Kam & Govender 1994. Weinberg et al 1994.…”

Section: Introductionmentioning

confidence: 99%

Evidence for the involvement of nitric oxide in cisplatin-induced toxicity in rats

et al. 1996

View full text Add to dashboard Cite

Cisplatin treatment of rats results into a significant increase in the activity of Ca(2+)-independent nitric oxide synthase (NOS) in kidneys and liver. Significant enhancement of lipid peroxidation in gastric mucosa, kidneys and liver was also observed. The administration of NG-nitro-L-arginine methyl ester, an inhibitor of NOS, markedly reduced renal and gastrointestinal toxicity, and also decreased the content of blood urea nitrogen, serum creatinine, and incidence of diarrhoea along with a significant inhibition in lipid peroxidation in the target organs. The present report, while demonstrating the beneficial effect of the blockade of NO pathways during cisplatin chemotherapy, may be helpful in developing strategies for combating some of the toxic side-effects of the drug.

show abstract

Nitric oxide: basic science and clinical applications

Cited by 41 publications

References 55 publications

Expression of three forms of nitric oxide synthase in peripheral nerve regeneration

Expression of three forms of nitric oxide synthase in peripheral nerve regeneration

Effects of Ginkgo biloba extract (EGb 761) on gene expression: Possible relevance to neurological disorders and age‐associated cognitive impairment

Evidence for the involvement of nitric oxide in cisplatin-induced toxicity in rats

Contact Info

Product

Resources

About