1996
DOI: 10.1016/0891-5849(96)00171-2
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Fetal growth retardation in rats may result from apoptosis: Role of peroxynitrite

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Cited by 63 publications
(33 citation statements)
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“…When we looked at previous studies that investigated the effects of various medications administered during the fetal period, we found that non-steroidal anti-inflammatory drugs at toxic doses caused intrauterine growth retardation (32,33) and nitric oxide synthase inhibitors resulted in fetal growth retardation by uteroplacental dysfunction (34,35). Further, Ishida et al (36) reported that DL-alpha-difluoromethyl orni- (9) f (10) m (2) f (5) m (20) f (13) m (9) f (10) m (2) f (5) m (20) f (13) m (9) f (10) m (2) f (5) m (20) f (13) Table 1c.…”
Section: Discussionmentioning
confidence: 99%
“…When we looked at previous studies that investigated the effects of various medications administered during the fetal period, we found that non-steroidal anti-inflammatory drugs at toxic doses caused intrauterine growth retardation (32,33) and nitric oxide synthase inhibitors resulted in fetal growth retardation by uteroplacental dysfunction (34,35). Further, Ishida et al (36) reported that DL-alpha-difluoromethyl orni- (9) f (10) m (2) f (5) m (20) f (13) m (9) f (10) m (2) f (5) m (20) f (13) m (9) f (10) m (2) f (5) m (20) f (13) Table 1c.…”
Section: Discussionmentioning
confidence: 99%
“… 4-þ ãðóïïó âîøëè aeèâîòíûå ñ ÍÌÏÊ, äîïîëíèòåëüíî ïî-ëó÷àâøèå ñ 1-ãî äíÿ áåðåìåííîñòè âìåñòî ïèòüåâîé âîäû äîíàòîð îêèñè àçîòà 0,2 % ðàñòâîð íèòðèòà íà-òðèÿ [15]. Êðûñû ñ ÍÌÏÊ è ââåäåíèåì íåñåëåêòèâíî-ãî èíãèáèòîðà ñèíòåçà îêèñè àçîòà ìåòèëîâîãî ýôèðà L-àðãèíèíà (L-NAME) (Sigma) âíóòðèìûøå÷íî â äîçå 10 ìã/êã [12] ñ 1 äíÿ áåðåìåííîñòè ñîñòàâèëè 5-þ ãðóïïó.…”
Section: ìåòîäû èññëåäîâàíèßunclassified
“…In the fetus exposed to an episode of ischemia, alteration of DNA can increase, in vivo, by a factor from 12 to 128 [25]. Despite active repair activities [19], some of the damaged DNA is subject to permanent alterations which can induce cellular apoptosis or tissue necrosis [26,27], fetal growth retardation [27], death of the embryo [28] or latent pathologies [29,30], some of which break out when the organism faces new disequilibria between ROS production and elimination, notably during postnatal life.…”
Section: Overview Of Radical Phenomenamentioning
confidence: 99%
“…ROS production in the pregnant woman or gestating laboratory animal A large set of factors can induce high steady rates of ROS (H 2 O 2 , O −• 2 and • NO) from the time of ovulation up to delivery: high rates of estrogens [14,31], cytokines, oncogenes and growth factor signaling [16], production by neutrophiles [8,32] or activation of membrane NADPH oxidases by contact between tissues from the embryo and mother [33]. High levels of • NO are also observed in the circulation of pregnant women [5,32] or gestating rats [27], notably produced by neutrophiles together with O −• 2 . ROS production by neutrophiles during gestation do not bear any relationship to their usual function, adherence, chemotaxis or phagocytosis [32].…”
Section: Ros Productionmentioning
confidence: 99%
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