The Nitric Oxide Theory of Aging Revisited

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dc.contributor.authorMcCann, Samuel M.
dc.contributor.authorMastronardi, Claudio
dc.contributor.authorDe Laurentiis, A.
dc.contributor.authorRettori, V.
dc.date.accessioned2015-12-08T22:20:41Z
dc.date.issued2005
dc.date.updated2015-12-08T08:32:39Z
dc.description.abstractBacterial and viral products, such as bacterial lipopolysaccharide (LPS), cause inducible (i) NO synthase (NOS) synthesis, which in turn produces massive amounts of nitric oxide (NO). NO, by inactivating enzymes and leading to cell death, is toxic not only to invading viruses and bacteria, but also to host cells. Injection of LPS induces interleukin (IL)-1β, IL-1α, and iNOS synthesis in the anterior pituitary and pineal glands, meninges, and choroid plexus, regions outside the blood-brain barrier. Thereafter, this induction occurs in the hypothalamic regions (such as the temperature-regulating centers), paraventricular nucleus (releasing and inhibiting hormone neurons), and the arcuate nucleus (a region containing these neurons and axons bound for the median eminence). Aging of the anterior pituitary and pineal with resultant decreased secretion of pituitary hormones and the pineal hormone melatonin, respectively, may be caused by NO. The induction of iNOS in the temperature-regulating centers by infections may cause the decreased febrile response in the aged by loss of thermosensitive neurons. NO may play a role in the progression of Alzheimer's disease and parkinsonism. LPS similarly activates cytokine and iNOS production in the cardiovascular system leading to coronary heart disease. Fat is a major source of NO stimulated by leptin. As fat stores increase, leptin and NO release increases in parallel in a circadian rhythm with maxima at night. NO could be responsible for increased coronary heart disease as obesity supervenes. Antioxidants, such as melatonin, vitamin C, and vitamin E, probably play important roles in reducing or eliminating the oxidant damage produced by NO.
dc.identifier.issn0077-8923
dc.identifier.urihttp://hdl.handle.net/1885/32102
dc.publisherNew York Academy of Sciences
dc.sourceAnnals of the New York Academy of Sciences
dc.subjectKeywords: alpha tocopherol; antioxidant; ascorbic acid; bacterium lipopolysaccharide; corticosterone; cyclic GMP; cytokine; gonadorelin; inducible nitric oxide synthase; leptin; mitochondrial enzyme; neurotransmitter; nitric oxide; nitric oxide synthase; prostaglan Bacterial lipopolysaccharide; Brain; Coronary heart disease; Cyclic GMP; Cyclooxygenase; Cytokines; Degenerative diseases; Hypothalamus; Infection; Inflammation; Nitric oxide synthase; Pineal gland; Pituitary gland; Stress
dc.titleThe Nitric Oxide Theory of Aging Revisited
dc.typeJournal article
local.bibliographicCitation.lastpage84
local.bibliographicCitation.startpage64
local.contributor.affiliationMcCann, Samuel M, Pennington Research Center
local.contributor.affiliationMastronardi, Claudio, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationDe Laurentiis, A, School of Medicine, UBA
local.contributor.affiliationRettori, V, University of Buenos Aires
local.contributor.authoremailu4776074@anu.edu.au
local.contributor.authoruidMastronardi, Claudio, u4776074
local.description.embargo2037-12-31
local.description.notesImported from ARIES
local.identifier.absfor110999 - Neurosciences not elsewhere classified
local.identifier.absseo970111 - Expanding Knowledge in the Medical and Health Sciences
local.identifier.ariespublicationu9505948xPUB88
local.identifier.citationvolume1057
local.identifier.doi10.1196/annals.1356.064
local.identifier.scopusID2-s2.0-32244435930
local.identifier.uidSubmittedByu9505948
local.type.statusPublished Version

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