由于脂质,碳水化合物和蛋白质代谢失调可以伴有甚至引起某些脉络膜视网膜的遗传变性,故一般看来很可能毯层视网膜变性(tapetoretinal degeneration),尤其是视网膜色素变性也归因于代谢紊乱,特别是酶的缺乏。其实,看来视网膜对各种遗传及代谢缺陷异常敏感。涉及色素性视网膜病变研究中的一个主要问题是可供研究的人眼组织不易得到;不可能切除一片视网膜,而活体眼不受到严重损害。动物模型及活体内测量各种机能反应虽增进了我们的认识与了解,然而、仍不能解释有关基本病理与生化异常的根本性问题。Levy强调:(1)构成40～60%光感受器的脂质的重要性;(2)杆体与色素上皮构成一种单独机能单位的概念;(3)影响这二种细胞代谢或与其相关的任何失调,均会破坏这种机能单 Since dyslipidemia of lipids, carbohydrates and proteins can be accompanied by or even cause genetic degeneration of some chorioretinal retinas, it is generally plausible that tapetoretinal degeneration, especially retinitis pigmentosa, is also due to metabolic disorders, Especially the lack of enzymes. In fact, it appears that the retina is unusually sensitive to a variety of genetic and metabolic defects. One of the major problems involved in the study of pigmented retinopathy is that the human eye tissue available for study is not readily available; it is not possible to excise a retina without serious damage to the living eye. Animal models and in vivo measurements of various functional responses have enhanced our understanding and understanding, however, and still fail to explain fundamental questions about underlying pathology and biochemical abnormalities. Levy emphasizes: (1) the importance of lipids that make up 40-60% of the photoreceptors; (2) the concept that the rod body and the pigment epithelium form a single functional unit; (3) the effects of any or all of the Disorders, will destroy this single function