母体疟疾感染时早期妊娠猕猴胎盘的氧化还原酶：组织化学定位

Saxena Nishi, Murthy P S R

Department of Zoology, School of Life Sciences, Dr. B.R. Ambedkar University, Agra, India.

J Vector Borne Dis. 2007 Jun;44(2):116-21.

BACKGROUND & OBJECTIVES: Early gestational malaria is more deleterious than late gestational infection. Still the pathophysiology of maternofoetal organ--the placenta in malaria remains almost unexplored during early gestation. Present study dealing with oxidoreductases in early gestational placenta during maternal malarial infection of Plasmodium cynomolgi bastianellii in rhesus monkeys was anticipated to provide a better insight into the functional impairment of this organ leading to foetal abnormalities.

METHODS

Three control and four experimental monkeys (Macaca mulatta) were quarantined for one month prior to experimentation. Experimental monkeys at 2- 2 1/2 months of gestation were inoculated with P. cynomolgi bastianellii. On attaining first peak of parasitaemia the placentae were collected from anesthetised animals. The snap-frozen, cryostat sections were subjected to histochemical localisation for 3 (or 17) beta-hydroxysteroid dehydrogenase (beta-HSD) [3 (or 17) beta-hydroxysteroid: NAD (P+) oxidoreductase, EC 1.1.1.51 hydroxysteroid dehydrogenases] and NADPH-tetrazolium reductase [NADPH: (acceptor) oxidoreductase, EC 1.6.99.1 NADPH-TR]. Comparative microscopy of control and malaria infected placental sections was performed and analysed.

RESULTS

A localised decrease in both the enzymes was observed in syncytiotrophoblast layer of malaria infected monkey placenta. The areas showing morphological damage of syncytiotrophoblast were also depicting gross reduction in NADPH-TR activity.

INTERPRETATION & CONCLUSION: The altered enzymatic activities [3 (or 17) beta-HSD and NADPH-TR] in malaria infected early gestational monkey placenta have been discussed in the light of placental function. It could be concluded by present studies that these alterations would affect the cellular metabolism especially steroidogenesis and detoxification process which in turn would affect the normal development of the foetus as well as maintenance of gestation.

背景与目的

妊娠早期疟疾比妊娠晚期感染更具危害性。然而，在妊娠早期，母婴器官——胎盘在疟疾中的病理生理学几乎仍未被探索。本研究旨在探讨恒河猴感染食蟹猴疟原虫巴斯蒂安内利株后，妊娠早期胎盘氧化还原酶的情况，以期更好地了解该器官功能受损导致胎儿异常的机制。

方法

在实验前，将3只对照猴和4只实验猴（猕猴）隔离1个月。对妊娠2至2个半月的实验猴接种食蟹猴疟原虫巴斯蒂安内利株。在疟原虫血症首次达到峰值时，从麻醉的动物身上采集胎盘。将速冻的胎盘制成低温切片，进行3（或l7）β-羟类固醇脱氢酶（β-HSD）[3（或l7）β-羟类固醇：NAD（P+）氧化还原酶，EC 1.1.1.51羟类固醇脱氢酶]和NADPH-四氮唑还原酶[NADPH：（受体）氧化还原酶，EC 1.6.99.1 NADPH-TR]的组织化学定位。对对照和疟疾感染胎盘切片进行比较显微镜观察和分析。