The Impact of Senile Cataract Maturity on Blood Oxidative Stress Markers and Glutathione-Dependent Antioxidants: Relations with Lens Variables

Abstract

The Impact of Senile Cataract Maturity on Blood Oxidative Stress Markers and Glutathione-Dependent Antioxidants: Relations with Lens VariablesOxidative stress is implicated in senile cataract (SC) genesis, although the impact of SC maturity on blood oxidative stress markers is unclear. Total hydroperoxides, malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) were measured in the blood and lens samples of patients having either immature (n=31) or mature SC (n=50), and in 22 blood samples from noncataract controls. Compared to controls, SC patients had higher plasma MDA and serum GST, and decreased plasma GR and GSH levels. Plasma GPx as well as hydroperoxides differed from control values only in patients with mature SC. The multivariate logistic regression analysis showed that the fall of plasma GR activity (OR 5.14; CI 1.82-14.51;p=0.0020), as well as serum GST activity (OR 3.84; CI 1.36-10.83;p=0.0108) were independently associated with the maturity of SC. Lens hydroperoxides, MDA and GST, showed no correlation with correspondent blood values, in contrast to GPx (r=0.715; p<0.001) and GR (r=0.703; p<0.001). This study showed that the severity of SC is associated with increased systemic oxidative stress, which could be due to the fall of GSH-dependent antioxidant enzymes activities.

Influence of cataract maturity on aqueous humor lipid peroxidation markers and antioxidant enzymes

“…The other reason is that in SC the antioxidant genes can be markedly downregulated, 29 and the progression of SC has already been associated with decreased GPx activity, both at local and systemic level. 2,3 Furthermore, lenses of acatalasemic mice were demonstrated to be almost as efficient in degrading the H 2 O 2 ex vivo as those of the wild type, 30 indicating that CAT itself may not be of critical importance for prevention of lens oxidative damage. In the current study, the average CAT activity in AH was 32 pmol/ml, and was unrelated to oxidative stress status and, as in a previous study, 5 unaffected by cataract maturity.…”

“…It is now well established that excess levels of ocular oxidants can cause damage to the lens and other tissues, which are implicated in normal ageing process and in pathogenesis of several eye diseases, such as pseudoexfoliation syndrome, diabetic retinopathy, glaucoma, and senile cataract (SC). [1][2][3][4][5][6][7] The toxicity of oxidants depends on their ability to induce cross-linking, aggregation, fragmentation, and insolubilization of structural proteins, inactivation of enzymes, and lipid peroxidation (LPO) of the membrane-bound polyunsaturated fatty acids (PUFA), leading to impaired cell function, apoptosis, and necrosis. 1,2 Unlike ocular tissues, AH contains only small quantities of proteins and antioxidant enzymes, and its antioxidant defense thus relies on unusually high levels of low-molecular weight antioxidants, mostly ascorbic acid, present at the level of B1 mM, even in SC.…”

Oxidative Stress in the Anterior Ocular Diseases: Diagnostic and Treatment

“…Malondialdehyde (MDA), a lipid peroxidation product, is considered a biomarker. An increase in MDA serum levels in patients with senile cataracts has been reported [208][209][210][211]. Studies performed in humans and animals concluded the increment in lens MDA concentration was higher in diabetic cataracts than in senile non-diabetic cataracts [212,213].…”

“…Studies performed in humans and animals concluded the increment in lens MDA concentration was higher in diabetic cataracts than in senile non-diabetic cataracts [212,213]. In addition, plasma glutathione peroxidase (GPx) and hydroperoxides seem to be associated with the severity of the cataract [211].…”

“…Kato, A., M. Ishihara, and N. Mizuki [197] Cataract IL-6, IL-8 and TNF-α Hamid et al [202] IL-6, IL-1β, CRP, and TNF-1α [203] IL-6 and s-ICAM-1 E K Klein et al [204] IFN-γ, IL-6, IL-13, IL-12, IL-10, IFN-α2, CCL2, CCL3, CCL4, CXCL8, CXCL9, CXCL10 Zheng, Y., et al [205] VEGF IL-10 Mitrovic et al [206] MDA Singh, S. [208][209][210][211] TGFβ and MMP-9 Alapure et al [214] 4. Treatment 4.1.…”