Espeel M, Depreter M, Nardacci R, D'Herde K, Kerckaert I, Stefanini S, Roels F
Department of Anatomy, Embryology and Histology, University of Gent, Belgium.
Microsc Res Tech. 1997 Dec 1;39(5):453-66. doi: 10.1002/(SICI)1097-0029(19971201)39:5<453::AID-JEMT8>3.0.CO;2-H.
Peroxisomes are single membrane-limited cell organelles that are involved in numerous metabolic functions. Peroxisomes do not contain DNA; the matrix and membrane proteins are encoded by the nuclear genome. It is assumed that new peroxisomes are formed by division of existing organelles. The present article gives an overview of microscopic studies and recent unpublished results dealing with peroxisome biogenesis in mammalian fetal liver and presents data on peroxisomes in oocytes. Cytochemical (catalase and D-aminoacid oxidase activity) and immunocytochemical data in rat and human liver (antigens of catalase, the three peroxisomal beta-oxidation enzymes, alanine: glyoxylate aminotransferase, peroxisomal membrane proteins with molecular weights of 42 and 70 kDa) indicate that during embryonic and fetal development the peroxisomal population undergoes a differentiation with respect to the composition of the matrix and to the size and number of the organelles. In the youngest stages, rare and small peroxisomes are present, into which the matrix components are imported in a sequential way. The import seems asynchronous in peroxisomes of the same hepatocyte. The size and number of the peroxisomes increase during liver development. In rat and human liver, no morphological or immunocytochemical evidence for an elaborate network of interconnected peroxisomes ("reticulum") was found. Instead, peroxisomes presented as individual organelles, which occasionally show membrane extensions. The importance of the metabolic functions of peroxisomes in human liver is emphasized by the peroxisomal disorders. In the liver of affected fetuses, the microscopic features associated with the defect can already be recognized; i.e., either catalase containing peroxisomes are absent and catalase is localized in the cytoplasm (in fetuses affected with Zellweger syndrome or with infantile Refsum disease) or peroxisomes are present but they are abnormally enlarged (e.g., a fetus affected with acyl-CoA oxidase deficiency). In the quail ovary, numerous peroxisomes are observed in the oocyte and in the granulosa cells during follicle maturation, but not in the full-grown egg. Thus, the mechanism of peroxisome inheritance remains unresolved.
过氧化物酶体是由单层膜包被的细胞器,参与多种代谢功能。过氧化物酶体不含DNA;其基质和膜蛋白由核基因组编码。据推测,新的过氧化物酶体是由现有细胞器分裂形成的。本文概述了关于哺乳动物胎儿肝脏过氧化物酶体生物发生的微观研究及近期未发表的结果,并展示了卵母细胞中过氧化物酶体的数据。大鼠和人类肝脏的细胞化学(过氧化氢酶和D - 氨基酸氧化酶活性)及免疫细胞化学数据(过氧化氢酶、三种过氧化物酶体β - 氧化酶、丙氨酸:乙醛酸转氨酶的抗原、分子量为42和70 kDa的过氧化物酶体膜蛋白)表明,在胚胎和胎儿发育过程中,过氧化物酶体群体在基质组成、细胞器大小和数量方面经历了分化。在最早期阶段,存在稀少且小的过氧化物酶体,基质成分以顺序方式导入其中。在同一肝细胞的过氧化物酶体中,导入似乎是异步的。在肝脏发育过程中,过氧化物酶体的大小和数量会增加。在大鼠和人类肝脏中,未发现存在精细的相互连接的过氧化物酶体网络(“网状结构”)的形态学或免疫细胞化学证据。相反,过氧化物酶体呈现为单个细胞器,偶尔会有膜延伸。过氧化物酶体疾病强调了过氧化物酶体在人类肝脏代谢功能中的重要性。在受影响胎儿的肝脏中,与缺陷相关的微观特征已经可以识别;即,要么不含过氧化氢酶的过氧化物酶体缺失,过氧化氢酶定位于细胞质中(在患有泽尔韦格综合征或婴儿型Refsum病的胎儿中),要么过氧化物酶体存在但异常增大(例如,患有酰基辅酶A氧化酶缺乏症的胎儿)。在鹌鹑卵巢中,在卵泡成熟过程中,卵母细胞和颗粒细胞中观察到大量过氧化物酶体,但在成熟卵中未观察到。因此,过氧化物酶体遗传机制仍未解决。