Lipid peroxidation and human cataractogenesis in diabetes and severe myopia

Simonelli, Francesca; Nesti, Anna; Pensa, M; Romano, Laura; Savastano, Silvia; Rinaldi, E; Auricchio, G

doi:10.1016/0014-4835(89)90088-2

Cited by 86 publications

(42 citation statements)

References 21 publications

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“…In addition, free radical scavengers have also been reported to prevent GC-induced cataract formation [64][65][66] by increasing GSH levels and decreasing LPO. Decreasing the levels of GSH, when reactive oxygen species are present, can trigger a cascade of further oxidative damage, such as LPO, which has been associated with the formation of cataracts in patients [67][68][69][70].…”

Section: Discussionmentioning

confidence: 99%

N-acetylcysteine amide protects against dexamethasone-induced cataract related changes in cultured rat lenses

Tobwala¹,

Pınarcı²,

Maddirala³

et al. 2014

ABC

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Glucocorticoids (GCs) are one of the most widely used immunosuppressive and anti-inflammatory agents. However, their long term and systemic use is associated with adverse drug reactions including posterior subcapsular cataracts as one of its ocular complications. Balanced redox state is crucial for maintenance of lens transparency, and a high content of glutathione (GSH) in the lens is believed to play a key role in doing so. Depletion of GSH is implicated in the etiopathogenesis of dexamethasone-induced cataracts and, therefore, the present study was sought to evaluate the efficacy of a novel thiol antioxidant, N-acetylcysteine amide (NACA), in preventing dexamethasone-induced cataractogenesis. Cataract formation was induced by incubation of rat lenses with 5 µM dexamethasone. To assess whether NACA had a significant impact on dexamethasone-induced cataracts, the rat lenses were divided into four groups: 1) control group (Dulbecco's Modified Eagle Medium (DMEM), 2) dexamethasone group (DMEM with 5 µM dexamethasone), 3) NACA-only group (50 µM NACA solution), and 4) NACA pretreatment group (50 µM NACA for 6 hours followed by 5 µM dexamethasone only for 18 hours). Lenses were cultured for 7 days at 37˚C under 5% CO 2 . Lenses were evaluated daily using a dissecting microscope and photographed and graded for the development of opacity. The rat lenses in both the control and the NACA-only groups were clear, whereas all lenses within the dexamethasone-only group developed well-defined cataracts. Overall observations indicated that NACA inhibits cataract formation by limiting lipid peroxidation and increasing the ratio of GSH/GSSG in lens. Therefore, NACA can be developed into a potential adjunctive therapeutic option for patients undergoing therapy with GCs to inhibit glucocorticoid-induced cataracts.

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Section: Discussionmentioning

confidence: 99%

N-acetylcysteine amide protects against dexamethasone-induced cataract related changes in cultured rat lenses

Tobwala¹,

Pınarcı²,

Maddirala³

et al. 2014

ABC

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“…The concentration of malondialdehyde in the human lens increases with age ( 33 ) and cataract (5,33,(46)(47)(48)(49)(50)(51)(52). The association between lens opacity and lipid oxidation was so convincing that Babizhayev et al ( 50 ) boldly proclaimed that lipid oxidation may be an initiating step in the pathogenesis of human cataract. Over a human lifetime, more than 40% of the lens phospholipids are degraded, forming deleterious oxidation products ( 53 ).…”

Section: Lipid Oxidationmentioning

confidence: 99%

Lipids and the ocular lens

Borchman

Yappert

2010

Journal of Lipid Research

141

133

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“…Lipid peroxidation has been associated with cataract formation [65][66][67]. Polyunsaturated fatty acids are susceptible to free radical attack, initiating a chain reaction that terminates in the formation of stable byproducts, such as malondialdehyde (MDA), which are used as markers of lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Prevention and reversal of selenite‐induced cataracts by N‐acetylcysteine amide in Wistar rats

Maddirala

Tobwala

Karacal

et al. 2016

Acta Ophthalmologica

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Background: The present study sought to evaluate the efficacy of N-acetylcysteine amide (NACA) eye drops in reversing the cataract formation induced by sodium selenite in male Wistar rat pups. Methods: Forty male Wistar rat pups were randomly divided into a control group, an N-acetylcysteine amide-only group, a sodium selenite-induced cataract group, and a NACA-treated sodium selenite-induced cataract group. Sodium selenite was injected intraperitoneally on postpartum day 10, whereas N-acetylcysteine amide was injected intraperitoneally on postpartum days 9, 11, and 13 in the respective groups. Cataracts were evaluated at the end of week 2 (postpartum day 14) when the rat pups opened their eyes. N-acetylcysteine amide eye drops were administered beginning on week 3 until the end of week 4 (postpartum days 15 to 30), and the rats were sacrificed at the end of week 4. Lenses were isolated and examined for oxidative stress parameters such as glutathione, lipid peroxidation, and calcium levels along with the glutathione reductase and thioltransferase enzyme activities. Casein zymography and Western blot of m-calpain were performed using the water soluble fraction of lens proteins. Results: Morphological examination of the lenses in the NACA-treated group indicated that NACA was able to reverse the cataract grade. In addition, glutathione level, thioltransferase activity, m-calpain activity, and m-calpain level (as assessed by Western blot) were all significantly higher in the NACA-treated group than in the sodium selenite-induced cataract group. Furthermore, sodium selenite-injected rat pups had significantly higher levels of malondialdehyde, glutathione reductase enzyme activity, and calcium levels, which were reduced to control levels upon treatment with NACA.

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Lipid peroxidation and human cataractogenesis in diabetes and severe myopia

Cited by 86 publications

References 21 publications

N-acetylcysteine amide protects against dexamethasone-induced cataract related changes in cultured rat lenses

N-acetylcysteine amide protects against dexamethasone-induced cataract related changes in cultured rat lenses

Lipids and the ocular lens

Prevention and reversal of selenite‐induced cataracts by N‐acetylcysteine amide in Wistar rats

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