Diamine oxidase in relation to diamine and polyamine metabolism

Sessa, Angela; Perin, Antonio

doi:10.1007/bf02005768

Cited by 51 publications

(25 citation statements)

References 110 publications

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“…Nilsson extremely rich in diamine oxidase [3,4], the enzyme is supposed to be synthesized by the enterocytes [5] and then transported to vascular binding sites from which it can be released by heparin [6,7]. It has been suggested that intestinal diamine oxidase exerts an important barrier function against diamines [8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of diamine oxidase promotes uptake of putrescine from rat small intestine

1996

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In blood from the portal vein of anaesthetized rats the levels of histamine and putrescine were 2-3-fold lower compared to arterial blood. Putrescine concentration was increased severalfold and the difference between portal and arterial blood abolished in animals pretreated with the specific diamine oxidase inhibitor aminoguanidine. Histamine concentration was 40% lower in portal compared to arterial blood in animals treated with the mast cell degranulator compound 48/80. In animals pretreated with aminoguanidine, compound 48/80 enhanced the level of histamine and no difference was observed between arterial and portal blood. The amounts of intravenously injected [14C]-labeled histamine was about 15% lower in portal compared to arterial blood. The uptake of [14C]-putrescine from the small intestine was estimated. In urine from animals pretreated with aminoguanidine the concentration of [14C]-putrescine was more than 40-times higher than in control animals corresponding to a calculated uptake of about 7% in aminoguanidine treated animals. Our results suggest that intestinal diamine oxidase clears the blood from diamines and prevents luminal uptake of putrescine.

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Section: Introductionmentioning

confidence: 99%

Inhibition of diamine oxidase promotes uptake of putrescine from rat small intestine

1996

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“…However, AG has also other pharmacologic actions that might contribute to its neu roprotective effects. For example, AG is a potent inhibi tor of diamine oxidase (Beaven et aI., 1969), an enzyme that participates in the degradation of histamine and polyamines (Sessa and Perin, 1994). The terminal oxi dative deamination of polyamines by diamine oxidase leads to the production of toxic aldehydes (Sessa and Perin, 1994), compounds that could potentially contrib ute to cerebral ischemic damage.…”

Section: I·mentioning

confidence: 99%

“…For example, AG is a potent inhibi tor of diamine oxidase (Beaven et aI., 1969), an enzyme that participates in the degradation of histamine and polyamines (Sessa and Perin, 1994). The terminal oxi dative deamination of polyamines by diamine oxidase leads to the production of toxic aldehydes (Sessa and Perin, 1994), compounds that could potentially contrib ute to cerebral ischemic damage. Because increased polyamine synthesis and degradation begins early after an ischemic insult (Paschen et al, 1993), it is unlikely that, under the experimental conditions of the present study, inhibition of diamine oxidase contributes to the protective effect of AG.…”

Section: I·mentioning

confidence: 99%

Delayed Treatment with Aminoguanidine Decreases Focal Cerebral Ischemic Damage and Enhances Neurologic Recovery in Rats

Nagayama

Zhang

Iadecola

1998

J Cereb Blood Flow Metab

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Summary: Delayed treatment with aminoguanidine (AG), a relatively selective inhibitor of inducible nitric oxide synthase, ameliorates brain damage produced by occlusion of the rat's middle cerebral artery (MCA). We investigated whether the protection exerted by AG is dose-dependent and whether it is associated with improved neurologic outcome. We also studied the effect of the timing of administration of AG relative to the induction of cerebral ischemia. Halothane-anesthetized sponta neously hypertensive rats underwent permanent MCA occlu sion distal to the lenticulostriate branches. Neurologic deficits were assessed daily by the postural reflex test and beam bal ance test. Infarct volume was determined in thionin-stained sections 96 hours after ischemia and values corrected for swell ing. Treatment with AG (intraperitoneally, twice daily), starting 24 hours after MCA occlusion, decreased neocortical infarct volume in comparison to vehicle-treated rats. After correction for swelling, the decrease was 8 ± 12% at 50 mg/kg (n = 8; P > .05; analysis of variance), 25 ± 13% at 100 mg/kg (n = 7; P We have previously shown that administration of ami noguanidine (AG), a compound that inhibits inducible nitric oxide synthase (iNOS), decreases the infarct result ing from transient or permanent occlusion of the middle cerebral artery (MCA) in rats Iadecola et al., 1995a;Zhang et al., 1996). AG blocks the increase in iNOS activity that follows focal cerebral isch- Abbreviations used: AG, aminoguanidine; AGE, advanced glycation end-product; eNOS, endothelial nitric oxide synthase; HSD, honestly significant difference; iNOS, inducible nitric oxide synthase; MCA, middle cerebral artery; SHR, spontaneously hypertensive rats. 1107< .05), 30 ± 16% at 200 mg/kg (n = 7; P < .05) and 32 ± 9% at 400 mg/kg (n = 5; P < .05). Twenty-four hours after induc tion of ischemia neurologic deficits scores did not differ be tween treated and untreated rats (P > .05). However, from 48 to 96 hours after ischemia, neurologic deficits improved signifi cantly in rats treated with AG (100 to 400 mg/kg) compared to rats in which vehicle was administered (P < .05). The decrease in neocortical infarct volume was greatest when AG (100 mg/ kg; twice daily) was administered 12 (26 ± 17%; n = 9) or 24 hours (25 ± 13; n = 7) after MCA occlusion. The findings show that AG decreases ischemic brain damage dose dependently and improves neurologic recovery. Delayed treat ment with AG may be a therapeutic strategy to selectively target the evolution of ischemic damage that occurs in the post-ischemic period.

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“…In the present study, the DMH protocol may not have elevated blood polyamines enough to cause anemia in the copper adequate rats. On the other hand, the DMH polyamine effect may have been amplified in the copper marginal rats, which showed low activities of diamine oxidase, an enzyme that catabolizes polyamines [27].…”

Section: Discussionmentioning

confidence: 99%

Long-term marginal copper intake by rats: Effects on copper enzyme activities and responses to dimethylhydrazine

DiSilvestro¹,

Wildman²,

Jalili³

et al. 2000

J. Trace Elem. Exp. Med.

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Diamine oxidase in relation to diamine and polyamine metabolism

Cited by 51 publications

References 110 publications

Inhibition of diamine oxidase promotes uptake of putrescine from rat small intestine

Inhibition of diamine oxidase promotes uptake of putrescine from rat small intestine

Delayed Treatment with Aminoguanidine Decreases Focal Cerebral Ischemic Damage and Enhances Neurologic Recovery in Rats

Long-term marginal copper intake by rats: Effects on copper enzyme activities and responses to dimethylhydrazine

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