Ostapenko I A
Vopr Med Khim. 1981;27(4):519-23.
A correlation was noted between alterations in activity of cGMP phosphodiesterase /PDE/ and in content of rhodopsin /R/ from rats of the Campbell strain with hereditary retina degeneration as well as from control animals of the Wistar strain. Dynamics of alterations in the PDE/R ratio was similar to both in impaired and healthy animals within the first 35 days of life. These data suggest that the decrease of the PDE activity in retina of the Campbell rats occurred due to destruction and removing of outer layer of photoreceptor cell segments, i.e. it was of the secondary nature rather than of primary pathogenetic importance. After 1.5 month of the life retina aqueous extract activated PDE of cyclic nucleotides in impaired rats, but did not cause inhibition as it was observed in healthy animals. The phenomenon appears to be due to various localization of PDE inhibitors and activators in retina as well as to destruction of the layer of rod outer segments in retina of impaired rats.
在患有遗传性视网膜变性的坎贝尔品系大鼠以及作为对照的Wistar品系动物中,观察到环磷酸鸟苷磷酸二酯酶(PDE)活性变化与视紫红质(R)含量之间存在相关性。在出生后的前35天内,PDE/R比值的变化动态在受损动物和健康动物中相似。这些数据表明,坎贝尔大鼠视网膜中PDE活性的降低是由于光感受器细胞节段外层的破坏和清除所致,即它是继发性的,而非原发性致病因素。在出生1.5个月后,受损大鼠视网膜水提取物可激活环核苷酸的PDE,但不像在健康动物中那样引起抑制作用。这种现象似乎是由于PDE抑制剂和激活剂在视网膜中的定位不同,以及受损大鼠视网膜中视杆细胞外节层的破坏所致。