Reduced and oxidized glutathione concentrations in the lenses of riboflavin-deficient rats.

Horiuchi, Saburo; Hirano, Hiroko; Ono, Shigeru

doi:10.3177/jnsv.30.401

Cited by 12 publications

(9 citation statements)

References 6 publications

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“…This would be perhaps due to difference in methodology used by different investigators. However, our values stand in good agreement with those (1.16±0.136 1u mol/ 100 mg lens) reported by Horiuchi et al [28]. Our observation of normal GSH levels in riboflavin deficiency is in agreement with that reported by Srivastava, and Beutler [7] in the lens.…”

Section: Pv Rao and Ks Bhat Discussionsupporting

confidence: 94%

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Influence Dietary Riboflavin Deficiency on Lenticular Glutathione Redox Cycle, Lipid Peroxidation, and Free Radical Scavengers in the Rat

Rao

Bhat

1989

J. Clin. Biochem. Nutr.

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(first set of animals) or 0.05 M sodium phosphate buffer, pH 7.2 (second set of animals) using a Potter/Elvehj am glass homogenizer. A 7.5% homogenate was prepared from two lenses (third set of animals) in 5% ice-cold TCA. Aliquots of J. Clin. Biochem. Nutr. INFLUENCE OF RIBOFLAVINDEFICIENCY ON RAT LENS 197 the lens homogenate (Tris-EFTA buffer) were analysed for GSH and GSSG measured fluorimetrically [11] in a Hitachi 650-lOS spectrofluorimeter and for total and non-protein sulfhydryl groups with Ellman's reagent [12]. Lipid peroxide level was estimated (in terms of malondialdehyde (MICA)) in the phosphate buffer by the thiobarbituric acid (TBA) reaction [13] and ascorbic acid in 5,000>< g supernatant of 5% TCA homogenate, using orthophosphoric acid, ferric chloride and aa '-dipyridyl [14]. The remaining homogenate (Tris-EFTA buffer) was centrifuged at 20.000>< g in a Sorvall RCSB super-speed centrifuge at 4°C for 30 min. The 20,000>< g supernatant was used for the assay of glutathione redox cycle enzymes. Glucose 6-phosphate dehydrogenase (G6PDH) was assayed spectrophotometrically as described by Selvaraj, and Bhat [15]. The reaction mixture contained in 1.2 ml: 50,u mol glycylglycine buffer (pH 8.7), 12 ,u mol KCl, 12 ,u mol MgC12, 3 ,u mol nicotinamide, 61u mol glucose 6-phosphate, and 75 1a l lens tissue supernatant. The reaction was started by adding 0.12 ,u mol NADP+. GSH-R was assayed by the method of Bayoumi, and osalki [16] as described elsewhere [9]. Glutathioneperoxidase (GSH-PX) was assayed as described by Hochstein and Utley [17] with the following modification: The reaction mixture contained in 1 ml: 50 ,u mol phosphate buffer (pH 7.2), 2.5 ,u mol GSH, 0.5 ,u mol NaN3, 0.3 ,u mol EFTA, 0.1 ,u mol NADPH, 0.5 IU GSH-R, and 75 ,u 1 supernatant (enzyme preparation, 1 : 5 dilution). The reaction mixture was incubated at 37°C for 10 min and the reaction started by the addition of 0.251a mol tert-butyl hydroperoxide. Catalase in the 750 X g supernatant fraction of the homogenate prepared in phosphate buffer was assayed polarographically as described by Goldstein [18] with a polarograph (YSI, Model 5301) equipped with an oxygen monitor (model 53) and a recorder (LKB 2210). The activity of superoxide dismutase (SOIL) in supernatant fractions of the lens homogenate (phosphate buffer) obtained by centrifugation at 35,000>< g and 0-4°C for 25 min was determined spectrophotometrically by measuring the inhibition of autooxidation of pyrogallol [19]. Protein concentration was measured by the method of Lowry et al. [20]. Statistical analysis. The data was analysed by one way analysis of variance. The mean differences were also further tested by Duncan's multiple range test. RESULTSThis study spans three different animal experiments in every one of which riboflavin-deficient rats showed a severe growth retardation, hair loss, and skin lesions, all of which are characteristic features of riboflavin deficiency.Ocular examination revealed severe corneal vascularization in riboflavindeficient rats (30%) as comp...

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Section: Pv Rao and Ks Bhat Discussionsupporting

confidence: 94%

“…A similar observation was also reported for erythrocyte GSH levels and HIP shunt [29,30]. However, Horiuchi et al [28] reported lowered GSH and increased GSSG in conjunction with lowered GSH-R activity in riboflavin-deficient rat lenses. The reasons for this difference is not clear at present.…”

Section: Pv Rao and Ks Bhat Discussionsupporting

confidence: 80%

Influence Dietary Riboflavin Deficiency on Lenticular Glutathione Redox Cycle, Lipid Peroxidation, and Free Radical Scavengers in the Rat

Rao

Bhat

1989

J. Clin. Biochem. Nutr.

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“…The reduction was higher in the riboflavin-treated group Hirano et al (34) Experimental Serum and lens GPx, SOD and GST activities, and lipid peroxide levels were assessed in riboflavin-deficient rats and riboflavin-sufficient control rats Serum and lens lipid peroxide levels were increased and lens GPx activity was decreased in riboflavin-deficient rats compared with those in the control rats. SOD and GST activities did not exhibit a significant change Horiuchi et al (25) Experimental Lens glutathione content was assessed in riboflavin-deficient rats and riboflavin-sufficient control rats…”

Section: Riboflavin At a Glancementioning

confidence: 99%

Riboflavin (vitamin B₂) and oxidative stress: a review

2014

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Oxidative stress is involved in the development of many chronic diseases. One of the main factors involved in oxidative stress reduction is increased antioxidant potential. Some nutrients such as vitamin C, vitamin E and carotenoids are known to act as antioxidants; however, riboflavin is one of the neglected antioxidant nutrients that may have an antioxidant action independently or as a component of the glutathione redox cycle. Herein, studies that have examined the antioxidant properties of riboflavin and its effect on oxidative stress reduction are reviewed. The results of the reviewed studies confirm the antioxidant nature of riboflavin and indicate that this vitamin can protect the body against oxidative stress, especially lipid peroxidation and reperfusion oxidative injury. The mechanisms by which riboflavin protects the body against oxidative stress may be attributed to the glutathione redox cycle and also to other possible mechanisms such as the conversion of reduced riboflavin to the oxidised form.

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“…Hwang and Kim [52] recently demonstrated that the transmittance of cross-linked corneas was 10-20% lower than that of control untreated corneas, concluding that riboflavin treatment exerts a protective effect against ultraviolet penetration in the rabbit cornea. However, riboflavin also has antioxidant properties and neutralizes lipid peroxidation throughout the glutathione redox cycle [53]. These two effects could explain the defensive role exerted by riboflavin in our experiments.…”

Section: Discussionmentioning

confidence: 63%

Corneal UV Protective Effects of a Topical Antioxidant Formulation: A Pilot Study on In Vivo Rabbits

Palazzo

Vizzarri

Ondruška

et al. 2020

IJMS

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This study aimed to evaluate the protective effect of a topical antioxidant and ultraviolet (UV) shielding action formulation containing riboflavin and D-α-tocopherol polyethylene glycol succinate (TPGS) vitamin E against corneal UV-induced damage in vivo rabbit eyes. In vivo experiments were performed using male albino rabbits, which were divided into four groups. The control group (CG) did not receive any UV irradiation; the first group (IG) was irradiated with a UV-B−UV-A lamp for 30 min; the second (G30) and third (G60) groups received UV irradiation for 30 and 60 min, respectively, and were topically treated with one drop of the antioxidant and shielding formulation every 15 min, starting one hour before irradiation, until the end of UV exposure. The cornea of the IG group showed irregular thickening, detachment of residual fragments of the Descemet membrane, stromal fluid swelling with consequent collagen fiber disorganization and disruption, and inflammation. The cornea of the G30 group showed edema, a mild thickening of the Descemet membrane without fibrillar collagen disruption and focal discoloration, or inflammation. In the G60 group, the cornea showed a more severe thickening, a more abundant fluid accumulation underneath the Descemet membrane with focal detachment, and no signs of severe tissue alterations, as were recorded in the IG group. Our results demonstrate that topical application of eye drops containing riboflavin and TPGS vitamin E counteracts UV corneal injury in exposed rabbits.

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Reduced and oxidized glutathione concentrations in the lenses of riboflavin-deficient rats.

Cited by 12 publications

References 6 publications

Influence Dietary Riboflavin Deficiency on Lenticular Glutathione Redox Cycle, Lipid Peroxidation, and Free Radical Scavengers in the Rat

Influence Dietary Riboflavin Deficiency on Lenticular Glutathione Redox Cycle, Lipid Peroxidation, and Free Radical Scavengers in the Rat

Riboflavin (vitamin B₂) and oxidative stress: a review

Corneal UV Protective Effects of a Topical Antioxidant Formulation: A Pilot Study on In Vivo Rabbits

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Reduced and oxidized glutathione concentrations in the lenses of riboflavin-deficient rats.

Cited by 12 publications

References 6 publications

Influence Dietary Riboflavin Deficiency on Lenticular Glutathione Redox Cycle, Lipid Peroxidation, and Free Radical Scavengers in the Rat

Influence Dietary Riboflavin Deficiency on Lenticular Glutathione Redox Cycle, Lipid Peroxidation, and Free Radical Scavengers in the Rat

Riboflavin (vitamin B2) and oxidative stress: a review

Corneal UV Protective Effects of a Topical Antioxidant Formulation: A Pilot Study on In Vivo Rabbits

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Riboflavin (vitamin B₂) and oxidative stress: a review