Green K, Costarides A P, Riley M V
Department of Ophthalmology, Medical College of Georgia, Augusta 30912.
Lens Eye Toxic Res. 1990;7(3-4):419-26.
Catalase inhibition leads to an increase in the t 1/2 for hydrogen peroxide loss from the anterior chamber and increased tissue damage. BCNU (1,3-bis-(2-chloroethyl)-l-nitrosourea) and BSO (buthionine sulfoxamine) were used to suppress glutathione reductase and glutathione synthesis, respectively. Intravitreal BSO (1 to 4 mg) reduced total glutathione levels of iris by 80%, and aqueous glutathione levels by 70%. BSO caused the t 1/2 for hydrogen peroxide disappearance from the anterior chamber to increase after 10 microliters of 10 mM peroxide was injected intracamerally but not after 25 or 50 mM peroxide injections. Catalase inhibition, however, had more influence at 50 mM than with 10 or 25 mM injections. The glutathione redox system is operative at low aqueous hydrogen peroxide concentrations and catalase is of greater importance at higher peroxide concentrations.
过氧化氢酶抑制会导致前房过氧化氢损失的半衰期延长,并增加组织损伤。分别使用卡莫司汀(1,3-双(2-氯乙基)-1-亚硝基脲)和丁硫氨酸亚砜胺来抑制谷胱甘肽还原酶和谷胱甘肽合成。玻璃体内注射丁硫氨酸亚砜胺(1至4毫克)可使虹膜总谷胱甘肽水平降低80%,房水谷胱甘肽水平降低70%。在前房内注射10微升10毫摩尔的过氧化物后,丁硫氨酸亚砜胺使前房过氧化氢消失的半衰期延长,但在注射25或50毫摩尔过氧化物后则不然。然而,过氧化氢酶抑制在注射50毫摩尔过氧化物时比注射10或25毫摩尔时影响更大。谷胱甘肽氧化还原系统在房水低浓度过氧化氢时起作用,而过氧化氢酶在较高过氧化物浓度时更为重要。