scholarly journals Lens Lipid Peroxides and Glutathione Concentrations in Diabetic Cataract

Author(s):  
D Özmen ◽  
I Mutaf ◽  
B Özmen ◽  
J Mentes ◽  
O Bayindir

This study aims to explore the role of reactive oxygen radicals in the genesis of diabetic cataract. Lipid peroxide (LPO) concentrations in senile ( n = 30) and diabetic ( n = 14) cataractous lenses, were determined as thiobarbituric acid-reactive substances (TBARS) by a method modified from Satoh and Yagi, and reduced glutathione (GSH) concentrations were measured according to Beutler. Lens LPO levels (mean, SD; nmol TBARS/g protein) were significantly higher in diabetics (107·54, 18·12) than senile cataractous subjects (53·54, 15·48) ( P < 0·0001). Lens GSH levels (mean, SD; nmol/g protein) showed no significant difference between diabetics (4·29, 2·05) and senile cataractous subjects (4·68, 3·12). These results suggest that free radical damage is more effective in the genesis of diabetic cataract than in senile cataract.

1998 ◽  
Vol 274 (2) ◽  
pp. G376-G384 ◽  
Author(s):  
Terry S. Legrand ◽  
Tak Yee Aw

We showed that hypoxia alters glutathione (GSH)-dependent detoxication and induces mucosal metabolic instability. To determine the impact of these changes and the role of reductant supply in intestinal lipid peroxide disposition, pair-fed (16 g/day) Sprague-Dawley rats were exposed to air (20.9% O2; n = 6) or 10% O2( n = 6) for 10 days. Jejunal and ileal everted sacs were exposed to 75 μM peroxidized fish oil with or without 10 mM glucose or 1 mM GSH. Peroxide transport was determined as the abluminal recovery of thiobarbituric acid-reactive substances. Peroxide recovery in hypoxic intestine was twice that in normoxic intestine. Addition of GSH and glucose did not affect peroxide recovery, indicating reduced intracellular GSH-dependent metabolism and enhanced output by the hypoxic intestine. Glucose uptake by normoxic and hypoxic intestine is similar, whereas its utilization for detoxication is decreased in hypoxic cells. Determination of NADPH supply indicates that decreased glucose availability for NADPH production during hypoxia impairs GSH disulfide reduction, compromises hydroperoxide metabolism, and increases peroxide output from hypoxic intestine.


2005 ◽  
Vol 2005 (3) ◽  
pp. 139-143 ◽  
Author(s):  
Ricardo González ◽  
Cheyla Romay ◽  
Aluet Borrego ◽  
Frank Hernández ◽  
Nelson Merino ◽  
...  

Cisplatin (CDDP), an anticancer drug, induces remarkable toxicity in the kidneys of animals and humans and it has been well documented that reactive oxygen species and the renal antioxidant system are strongly involved in acute renal damage induced by CDDP. The aim of the present study was to investigate whether or not the renal antioxidant system plays also an important role in chronic renal damage induced by repeated doses of CDDP (1 mg/kg intraperitoneally twice weekly during 10 weeks in rats). In order to elucidate it, serum creatinine and urea levels, renal glutathione and thiobarbituric acid-reactive substances (TBARS) content, as well as renal superoxide dismutase and glutathione peroxidase activities were measured in the kidney homogenates of chronically CDDP-treated rats and additionally histological studies were performed in the rat kidneys. The chronic treatment with CDDP induced a significant increase in creatinine and urea levels in serum, but the other parameters mentioned above were not significantly modified as compared to the values in nontreated rats. Taking into account these results, we conclude that chronic CDDP administration induces also severe nephrotoxicity, in contrast to CDDP acute application, without any significant modification in the activity of relevant antioxidant enzymes such as superoxide dismutase and glutathione peroxidase, renal glutathione and lipid peroxides, by which the role of the antioxidant system in chronic nephrotoxicity induced by CDDP in rats is uncertain.


2020 ◽  
Vol 16 (5) ◽  
pp. 743-748
Author(s):  
Ana R.S. de Oliveira ◽  
Kyria J.C. Cruz ◽  
Jennifer B.S. Morais ◽  
Juliana S. Severo ◽  
Jéssica B. Beserra ◽  
...  

Background: The role of minerals in preventing the generation of oxidative stress in obese individuals has been evaluated. Magnesium is an antioxidant nutrient and a cofactor of enzymes involved in the cell membrane stabilization, attenuating the effects of oxidative stress. Objective: To evaluate the association between magnesium and concentrations of thiobarbituric acid reactive substances (TBARS) in patients with obesity and eutrophic women. Methods: A cross-sectional study was conducted with 73 women, divided into two groups: case group (patients with obesity, n=27) and control group (eutrophic women, n=46). Measurements of body mass index and waist circumference were performed. Dietary magnesium intake was assessed by the three-day food record using the NutWin software. Urinary magnesium concentration was measured by atomic absorption spectrophotometry method. Plasma concentrations of thiobarbituric acid reactive substances (TBARS) were also determined. Results: Mean values of dietary magnesium intake were 161.59 ± 60.04 and 158.73 ± 31.96 for patients with obesity and control group, respectively, with no significant difference between the groups studied (p >0.05). The value of urinary excretion of magnesium was lower than the reference values in both groups, with no significant difference between the groups studied (p >0.05). The plasma concentration of thiobarbituric acid reactive substances was significantly higher in patients with obesity compared to the control group (p <0.001). There was no correlation between levels of magnesium biomarkers and the concentration of TBARS (p >0.05). Conclusion: Patients with obesity showed a reduced dietary magnesium intake which seems to induce hypomagnesuria as a compensatory mechanism. The marker of oxidative stress evaluated in this study was not influenced by magnesium.


2012 ◽  
Vol 1 (10) ◽  
pp. 79 ◽  
Author(s):  
G. Raja* ◽  
Ivvala Anand Shaker ◽  
Inampudi Sailaja ◽  
R. Swaminathan ◽  
S. Saleem Basha ◽  
...  

Natural antioxidants can protect the human body from free radicals and retard the progress of many chronic diseases as well as lipid oxidative rancidity in foods. The role of antioxidants has protected effect against free radical damage that may cause many diseases including cancer. Primary sources of naturally occurring antioxidants are known as whole grains, fruits, and vegetables. Several studies suggest that regular consumption of nuts, mostly walnuts, may have beneficial effects against oxidative stress mediated diseases such as cardiovascular disease and cancer. The role of antioxidants has attracted much interest with respect to their protective effect against free radical damage that may cause many diseases including cancer. Juglans regia L. (walnut) contains antioxidant compounds, which are thought to contribute to their biological properties. Polyphenols, flavonoids and flavonols concentrations and antioxidant activity of Leaves, Stems and Nuts extract of Juglans regia L. as evaluated using DPPH, ABTS, Nitric acid, hydroxyl and superoxide radical scavenging activity, lipid peroxidation and total oxidation activity were determined. The antioxidant activities of Leaves, Stems and Nuts extract of Juglans regia L. were concentration dependent in different experimental models and it was observed that free radicals were scavenged by the test compounds in all the models.


2009 ◽  
Vol 62 (11-12) ◽  
pp. 578-581
Author(s):  
Vesna Marjanovic ◽  
Vidosava Djordjevic ◽  
Goran Marjanovic

Introduction. The appearance and intensity of oxidative stress were analyzed in the course of mechanical ventilation and parameters that could point toward potential lung damage. Material and methods. In three time intervals on day 1, 3 and 7 of mechanical ventilation, parameters such as: triglycerides, cholesterol, lactate, serum lactic dehydrogenase, acid-base balance and lipid peroxidation products - thiobarbituric acid reactive substances, were followed in 30 patients with head injuries. Results. A decrease in the level of partial oxygen pressure (PaO2) (p<0.01) and PaO2/FiO2 index (p<0.05) in arterial blood was recorded on day 3 of mechanical ventilation. This was accompanied with an increase in alveolar-arterial difference (AaDO2) (p<0.05), thiobarbituric acid reactive substances (p<0.001) and lactic dehydrogenase (p<0.001) comparing to day 1 of mechanical ventilation. The patients with initial PaO2>120 mmHg, had significant increase of thiobarbituric acid reactive substances and AaDO2 (p<0.05) and fall of PaO2 (p<0.001) on day 3 of mechanical ventilation. Conclusion. Oxidative stress and lipid peroxide production are increased during third day of mechanical ventilation leading to disruption of oxygen diffusion through alveolar-capillary membrane and reduction of parameters of oxygenation.


Author(s):  
Perin Vural ◽  
Cemil Akgül ◽  
Mukaddes Canbaz

Background: Oxidative stress has been implicated in the pathogenesis of ageing and menopause, and can arise through the increased production of lipid peroxides and/or a deficiency of antioxidant defence. Aim: To investigate the effects of the menopause and tibolone treatment (2.5 mg/day for six months) on plasma antioxidants and lipid peroxidation. Methods: Plasma concentrations of ascorbic acid, α-tocopherol, total thiol groups, caeruloplasmin, erythrocyte glutathione (GSH) and malondialdehyde (MDA) were measured in 24 postmenopausal and 24 premenopausal healthy women. Results: Data analysis indicates a significant decrease in plasma ascorbic acid, α-tocopherol, total thiol groups, caeruloplasmin, erythrocyte GSH and a significant increase in lipid peroxides (expressed as MDA concentrations) in postmenopausal women. There was no significant difference between control and study groups in the mean plasma caeruloplasmin concentrations. It was found that there is a significant increase in α-tocopherol and significant decrease in lipid peroxide concentrations in postmenopausal after tibolone treatment. Conclusions: The menopause is associated with an increase in oxidative stress and a decrease of some antioxidants, such as ascorbic acid, α-tocopherol, total thiols and erythrocyte GSH. Tibolone treatment leads to a decrease in concentrations of plasma lipid peroxide, probably by stimulating direct and indirect mechanisms of tocopherol regeneration and increasing plasma concentrations of vitamin E. However, due to the relatively small numbers involved this study can be regarded as a pilot. Further studies performed on a larger scale are necessary to establish the exact mechanisms of tibolone in inhibiting oxidative stress in postmenopausal women.


1995 ◽  
Vol 167 (5) ◽  
pp. 610-617 ◽  
Author(s):  
Robin G. McCreadie ◽  
Elizabeth MacDonald ◽  
David Wiles ◽  
Graham Campbell ◽  
John R. Paterson

BackgroundTardive dyskinesia (TD) may be mediated through free radical damage to neurons. Plasma lipid peroxide levels are a measure of radical damage to fats. Vitamin E is a free radical scavenger.MethodOne hundred and twenty-eight schizophrenic patients were examined for TD using the Abnormal Involuntary Movements Scale. Blood samples were taken to measure plasma lipid peroxide, serum vitamin E and cholesterol, and vitamin Exholesterol ratios. Twenty-four patients were also examined in October 1993, January 1994, and April 1994. Biochemical results were compared in 81 patients and 79 normal subjects.ResultsPatients with and without TD did not differ in median plasma lipid peroxide and serum vitamin E levels, or vitamin Exholesterol ratios. Correlations between seasonal change scores in TD and biochemical measurements were low. Lipid peroxide levels were higher and vitamin Exholesterol ratios lower in patients than in normal subjects. Vitamin E levels were lowest in in-patients and in those living in supported accommodation.ConclusionsThe results do not support the hypothesis that TD is mediated through free radical damage to neurons, but suggest increased free radical activity in schizophrenia.


1995 ◽  
Vol 147 (2) ◽  
pp. 361-365 ◽  
Author(s):  
T Mano ◽  
R Sinohara ◽  
Y Sawai ◽  
N Oda ◽  
Y Nishida ◽  
...  

Abstract To determine how lipid peroxides and free radical scavengers are changed in the brain of hyper- or hypothyroid rats, we examined the behavior of lipid peroxide and free radical scavengers in the cerebral cortex of aged (1·5 years old) rats that had been made hyper- or hypothyroid by the administration of thyroxine or methimazol for 4 weeks. Concentrations of catalase, Mn-superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were increased in hyperthyroid rats compared with euthyroid rats. Concentrations of total SOD, Cu,Zn-SOD and GSH-PX were increased but that of Mn-SOD was decreased in hypothyroid animals. There were no differences among hyperthyroid, hypothyroid and euthyroid rats in the levels of coenzymes 9 or 10. The concentration of lipid peroxides, determined indirectly by the measurement of thiobarbituric acid reactants, was decreased in hyperthyroid rats but not in hypothyroid rats when compared with euthyroid animals. These findings suggest that free radicals and lipid peroxides are scavenged to compensate for the changes induced by hyper- or hypothyroidism. Journal of Endocrinology (1995) 147, 361–365


1960 ◽  
Vol 38 (9) ◽  
pp. 957-964 ◽  
Author(s):  
C. C. Tsen ◽  
H. B. Collier

Erythrocytes from rats on tocopherol-deficient and tocopherol-supplemented diets gave similar low values for lipid peroxides by the thiobarbituric acid test. Treatment of the cells from tocopherol-deficient rats with dialuric acid caused a marked increase in lipid peroxides and this closely paralleled the degree of hemolysis. Shaking of the red cells from tocopherol-deficient animals in an atmosphere of oxygen also resulted in a slow lipid peroxidation which again paralleled the degree of hemolysis. Addition of α-tocopherol to a suspension of erythrocytes from tocopherol-deficient rats decreased or completely prevented (depending upon concentration) hemolysis by dialuric acid and also decreased lipid peroxide formation.It is concluded that dialuric acid probably acts by catalyzing the formation of lipid peroxides in the unsaturated lipids of the membrane of erythrocytes from tocopherol-deficient animals. Tocopherol presumably inhibits peroxide formation, and therefore hemolysis, by virtue of its antioxidant action.


1991 ◽  
Vol 37 (10) ◽  
pp. 1756-1758 ◽  
Author(s):  
M A Arshad ◽  
S Bhadra ◽  
R M Cohen ◽  
M T Subbiah

Abstract Peroxidation of lipids is believed to play a key role in various degenerative diseases. However, few simple tests are able to detect individual susceptibility or resistance to peroxidation. Measurement of the basal concentrations of lipid peroxides in plasma is not satisfactory because they are so low. Therefore, we developed a test to determine susceptibility of whole plasma to metal/H2O2-catalyzed peroxidation. Incubation of 300-500 microL of plasma with H2O2/cupric acetate resulted in the formation of products from fatty acids (malonaldehyde, measured by thiobarbituric acid assay) and cholesterol (predominantly cholest-3,5-dien-7-one, measured by gas-liquid chromatography). In the presence of Cu2+, formation of malonaldehyde and cholest-3,5-dien-7-one increased at least 10-fold over basal values. Lipid peroxide (malonaldehyde) and cholesterol oxide concentrations after peroxidation were significantly higher (P less than 0.01) in diabetic plasma than in normal plasma. Because susceptibility to plasma peroxidation represents a balance between pro-oxidant factors and antioxidant protection, this test may be useful in determining individual susceptibility to peroxidation as influenced by nutritional and clinical status.


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