Protective effects of ebselen on sodium-selenite-induced experimental cataract in rats

Aydemir, Orhan; Güler, Mete; Kaya, Mehmet; Deniz, Nurettin; Üstündağ, Bilal

doi:10.1016/j.jcrs.2012.07.022

Cited by 13 publications

(10 citation statements)

References 19 publications

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“…3) when compared to control group lenses, indicating increased lipid peroxidation in the Na 2 SeO 3 group. This observation is consistent with other studies that reported increased lipid peroxidation upon treatment with Na 2 SeO 3 [13, 14, 19, 23, 30, 60, 61]. NACA was able to decrease the lipid peroxidation induced by Na 2 SeO 3 by providing adequate amounts of GSH, which is a substrate for the glutathione peroxidase-catalyzed reduction of hydroperoxides.…”

Section: Discussionsupporting

confidence: 92%

“…This is likely achieved through several processes: supplying cysteine for GSH biosynthesis, reducing extracellular cystine to cysteine [59], and converting GSSG to GSH by non-enzymatic thiol disulfide exchange [31]. Our results are in agreement with previous studies that reported a decrease in GSH levels upon Na 2 SeO 3 treatment in animal models [14, 19, 60–64]. …”

Section: Discussionsupporting

confidence: 91%

“…Since oxidative stress is implicated in cataract formation, application of an antioxidant capable of successfully penetrating the lens tissue represents a logical approach to counteract oxidation-related cataractogenesis. Several compounds with antioxidant properties have been reported to prevent selenite-induced cataracts, such as resveratrol [12], saffron [13], ellagic acid [14], garlic [15], melatonin [16], drevogenin D [17], caffeine [18], ebselen [19], lycopene in vivo [20], N-acetyl-L-carnitine in vitro and in vivo [21–23], and Ocimum sanctum in vivo and ex vivo [24]. In fact, N-acetylcysteine (NAC), a glutathione (GSH) prodrug, has previously been tried in selenite-induced cataracts in vivo [25] and was shown to prevent oxidative damage to the lens, slowing down cataractogenesis.…”

Section: Introductionmentioning

confidence: 99%

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

Maddirala¹,

Tobwala²,

Karacal³

et al. 2017

BMC Ophthalmol

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BackgroundThe 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.MethodsForty 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.ResultsMorphological 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.ConclusionsThe data suggest that NACA has the potential to significantly improve vision and decrease the burden of cataract-related loss of function. Prevention and reversal of cataract formation could have a global impact. Development of pharmacological agents like NACA may eventually prevent cataract formation in high-risk populations and may prevent progression of early-stage cataracts. This brings a paradigm shift from expensive surgical treatment of cataracts to relatively inexpensive prevention of vision loss.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

Maddirala¹,

Tobwala²,

Karacal³

et al. 2017

BMC Ophthalmol

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 91%

“…Since oxidative stress is implicated in cataract formation, application of an antioxidant capable of successfully penetrating the lens tissue represents a logical approach to counteract oxidation-related cataractogenesis. Several compounds with antioxidant properties have been reported to prevent selenite-induced cataracts, such as resveratrol [12], saffron [13], ellagic acid [14], garlic [15], melatonin [16], drevogenin D [17], caffeine [18], ebselen [19], lycopene in vivo [20], N-acetyl-L-carnitine in vitro and in vivo [21][22][23], and Ocimum sanctum in vivo and ex vivo [24]. In fact, N-acetylcysteine (NAC), a glutathione (GSH) prodrug, has previously been tried in selenite-induced cataracts in vivo [25] and was shown to prevent oxidative damage to the lens, slowing down cataractogenesis.…”

mentioning

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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Selenite and ebselen supplementation attenuates d-galactose-induced oxidative stress and increases expression of SELR and SEP15 in rat lens

et al. 2016

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Selenite and ebselen supplementation has been shown to possess anti-cataract potential in some experimental animal models of cataract, however, the underlying mechanisms remain unclear. The present study was designed to evaluate the anti-cataract effects and the underlying mechanisms of selenite and ebselen supplementation on galactose induced cataract in rats, a common animal model of sugar cataract. Transmission electron microscopy images of lens fiber cells (LFC) and lens epithelial cells (LEC) were observed in D-galactose-induced experimental cataractous rats treated with or without selenite and ebselen, also redox homeostasis and expression of proteins such as selenoprotein R (SELR), 15kD selenoprotein (SEP15), superoxide dismutase 1 (SOD1), catalase (CAT), β-crystallin protein, aldose reductase (AR) and glucose-regulated protein 78 (GRP78) were estimated in the lenses. The results showed that D-galactose injection injured rat lens and resulted in cataract formation; however, selenite and ebselen supplementation markedly alleviated ultrastructural injury of LFC and LEC. Moreover, selenite and ebselen supplementation could mitigate the oxidative damage in rat lens and increase the protein expressions of SELR, SEP15, SOD1, CAT and β-crystallin, as well as decrease the protein expressions of AR and GRP78. Taken together, these findings for the first time reveal the anti-cataract potential of selenite and ebselen in galactosemic cataract, and provide important new insights into the anti-cataract mechanisms of selenite and ebselen in sugar cataract.

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Protective effects of ebselen on sodium-selenite-induced experimental cataract in rats

Abstract: No author has a financial or proprietary interest in any material or method mentioned.

Cited by 13 publications

References 19 publications

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

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

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

Selenite and ebselen supplementation attenuates d-galactose-induced oxidative stress and increases expression of SELR and SEP15 in rat lens

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