The endopeptidase-resistant protein fraction from human cataractous lenses

Dillon, James; Castineiras, S.Garcia; Santiago, Marely; Spector, Abraham

doi:10.1016/0014-4835(84)90118-0

Cited by 17 publications

(6 citation statements)

References 21 publications

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“…Judging by the elution position of the peak relative to the elution position of standard peptides under identical conditions, the average apparent molecular weight of the modified species comprising this fraction was calculated to be approximately 2-3 000 Da. Similar data have been obtained by others (Dillon et al, 1984). The broad coloured peptide peak was collected and dried prior to subsequent digestion by pronase.…”

Section: Resultsmentioning

confidence: 76%

Molecular Evidence for the Involvement of Alpha Crystallin in the Colouration/Crosslinking of Crystallins in Age-related Nuclear Cataract

Chen

Reid

Simpson

et al. 1997

Experimental Eye Research

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Section: Resultsmentioning

confidence: 76%

Molecular Evidence for the Involvement of Alpha Crystallin in the Colouration/Crosslinking of Crystallins in Age-related Nuclear Cataract

Chen

Reid

Simpson

et al. 1997

Experimental Eye Research

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“…The incubation of bovine α -crystallins with low concentrations of 3-HK causes protein cross-linking and oxidation of methionine and tryptophan residues [93], indicating that the protein damage likely results from generation of reactive oxygen species. In the human lens, these reactions have been associated with both aging [94] and cataractous processes [95]. Also, it was shown that 3-HK and 3-HA provoke protein oxidative damage and induce apoptosis characterized by chromatin condensation and internucleosomal DNA cleavage in PC12, GT1-7, and SK-N-SH cells [92, 96–98].…”

Section: Metabolites With Redox and Neuroactive Propertiesmentioning

confidence: 99%

Kynurenines with Neuroactive and Redox Properties: Relevance to Aging and Brain Diseases

Ocampo

Huitrón

González-Esquivel

et al. 2014

Oxidative Medicine and Cellular Longevity

105

119

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The kynurenine pathway (KP) is the main route of tryptophan degradation whose final product is NAD+. The metabolism of tryptophan can be altered in ageing and with neurodegenerative process, leading to decreased biosynthesis of nicotinamide. This fact is very relevant considering that tryptophan is the major source of body stores of the nicotinamide-containing NAD+ coenzymes, which is involved in almost all the bioenergetic and biosynthetic metabolism. Recently, it has been proposed that endogenous tryptophan and its metabolites can interact and/or produce reactive oxygen species in tissues and cells. This subject is of great importance due to the fact that oxidative stress, alterations in KP metabolites, energetic deficit, cell death, and inflammatory events may converge each other to enter into a feedback cycle where each one depends on the other to exert synergistic actions among them. It is worth mentioning that all these factors have been described in aging and in neurodegenerative processes; however, has so far no one established any direct link between alterations in KP and these factors. In this review, we describe each kynurenine remarking their redox properties, their effects in experimental models, their alterations in the aging process.

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“…In the human lens, these reactions have been associated with aging and cataractous processes(134). Such modifications of proteins account for fiber cell apoptosis(15), epithelial cell apoptosis(16), and cataract formation in the mouse lens(15, 16).…”

Section: Kynurenine Pathwaymentioning

confidence: 99%

Tryptophan-kynurenine pathway is dysregulated in inflammation and immune activation

Liu²,

et al. 2015

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The kynurenine (Kyn) pathway is the major route for tryptophan (Trp) metabolism, and it contributes to several fundamental biological processes. Trp is constitutively oxidized by tryptophan 2, 3-dioxygenase in liver cells. In other cell types, it is catalyzed by an alternative inducible indoleamine-pyrrole 2, 3-dioxygenase (IDO) under certain pathophysiological conditions, which consequently increases the formation of Kyn metabolites. IDO is up-regulated in response to inflammatory conditions as a novel marker of immune activation in early atherosclerosis. Besides, IDO and the IDO-related pathway are important mediators of the immunoinflammatory responses in advanced atherosclerosis. In particular, Kyn, 3-hydroxykynurenine, and quinolinic acid are positively associated with inflammation, oxidative stress (SOX), endothelial dysfunction, and carotid artery intima-media thickness values in end-stage renal disease patients. Moreover, IDO is a potential novel contributor to vessel relaxation and metabolism in systemic infections, which is also activated in acute severe heart attacks. The Kyn pathway plays a key role in the increased prevalence of cardiovascular disease by regulating inflammation, SOX, and immune activation.

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The endopeptidase-resistant protein fraction from human cataractous lenses

Cited by 17 publications

References 21 publications

Molecular Evidence for the Involvement of Alpha Crystallin in the Colouration/Crosslinking of Crystallins in Age-related Nuclear Cataract

Molecular Evidence for the Involvement of Alpha Crystallin in the Colouration/Crosslinking of Crystallins in Age-related Nuclear Cataract

Kynurenines with Neuroactive and Redox Properties: Relevance to Aging and Brain Diseases

Tryptophan-kynurenine pathway is dysregulated in inflammation and immune activation

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