scholarly journals Effect of combined G6PD deficiency and diabetes on protein oxidation and lipid peroxidation

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Naif S. Karadsheh ◽  
Nisreen A. Quttaineh ◽  
Salem N. Karadsheh ◽  
Mohammad El-Khateeb
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Oxidation ◽  
G6pd Deficiency ◽  
Fold Increase ◽  
Protein Carbonyl ◽  
The Other ◽  
Diabetic Patients ◽  
Oxidative Markers ◽  
Other Hand

Abstract Background Oxidative Stress, an imbalance in the pro-oxidant/antioxidant homeostasis, occurs in many physiological and non-physiological processes and several human diseases, including diabetes mellitus (DM) and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Since the incidence of G6PD deficiency in Jordan and many parts of the world is high, this study aimed to measure the effect of G6PD deficiency on the oxidative markers and the antioxidant glutathione (GSH) in diabetic and non-diabetic individuals. Methods Whole blood G6PD deficiency was screened by the fluorescent spot method, and erythrocyte G6PD activity was determined using a quantitative assay. Since protein carbonyl (PC) and malondialdehyde (MDA) are the most widely measured markers for protein and lipid oxidation, respectively, plasma PC and MDA, in addition to blood GSH were determined by spectrophotometric assays, as biomarkers of oxidative stress. Results The incidence of G6PD deficiency among the diabetic subjects was 15%. PC level in patients with diabetes and in G6PD-deficient subjects was 5.5 to 6-fold higher than in non-diabetic subjects with sufficient G6PD levels (p<0.001). This fold increase was doubled in diabetic patients with G6PD deficiency (p<0.001). Furthermore, the MDA level was significantly increased by 28-41% in G6PD-deficient, diabetics with sufficient G6PD, and diabetics with G6PD deficiency compared to MDA level in non-diabetic with sufficient G6PD. On the other hand, GSH was significantly reduced to half in G6PD-deficient subjects and in diabetics with G6PD-deficiency. Conclusions The results showed that diabetes and G6PD deficiency increased protein oxidation and lipid peroxidation. However, the combination of both disorders has an additive effect only on protein oxidation. On the other hand, GSH level is only reduced in G6PD deficiency. In addition, diabetes and G6PD deficiency appear to be genetically linked since the incidence of G6PD deficiency among people with diabetes is more than the general population.

Effect of Combined G6PD Deficiency and Diabetes on Protein Oxidation and Lipid Peroxidation.

2020 ◽  
Author(s):  
Naif S Karadsheh ◽  
Nisreen A. Quttaineh ◽  
Salem N. Karadsheh ◽  
Mohammad El-Khateeb
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lipid Oxidation ◽  
Protein Oxidation ◽  
G6pd Deficiency ◽  
Spectrophotometric Assay ◽  
Oxidative Markers ◽  
High Incidence ◽  
Protein And Lipid Oxidation ◽  
Biomarkers Of Oxidative Stress

Abstract Oxidative Stress, an imbalance in the pro oxidant / antioxidant homeostasis occurs by a large number of physiological and nonphysiological processes and in several human diseases including diabetes.The use of protein carbony protein (PC) and malanodialdehyde (MDA) as biomarkers of oxidative stress are the most widely measured markers for protein and lipid oxidation. These are measured by spectrophotometric assay. the aim of the study is to measure the effect of G6PD – deficiency on the oxidative markers and the antioxidant GSH in diabetic and non diabetic individuals because of the high incidence of G6PD – deficiency in Jordan and many parts of the worldThe results show that diabetes and/or G6PD deficiency are positively connected to protein and lipid oxidation. The effect is additive in protein oxidation when both disorders are present. The antioxidant, GSH level, is not affected by diabetes but reduced to 50% by G6PD deficiency.

Lipid Peroxidation, Protein Oxidation, Gelatinases, and Their Inhibitors in a Group of Adults with Obesity

2019 ◽  
Vol 51 (06) ◽  
pp. 389-395 ◽  
Author(s):  
Gregorio Caimi ◽  
Baldassare Canino ◽  
Maria Montana ◽  
Caterina Urso ◽  
Vincenzo Calandrino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Oxidation ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
The Body ◽  
Control Group ◽  
The Matrix ◽  
Markers Of Oxidative Stress ◽  
Obese Subjects

AbstractThe association between obesity and cardiovascular diseases has a multifactorial pathogenesis, including the synthesis of inflammatory molecules, the increase in oxidative stress and the dysregulation of the matrix metalloprotease (MMP) concentration and activity. In a group of adults with obesity, divided in 2 subgroups according to the body mass index (BMI), we examined lipid peroxidation, expressed as thiobarbituric acid-reactive substances (TBARS), protein oxidation, expressed as protein carbonyl groups (PCs), plasma gelatinases (MMP-2 and MMP-9), and their tissue inhibitors (TIMP-1 and TIMP-2). In the whole group, as well as in the 2 subgroups (with BMI 30–35 or BMI>35) of obese subjects, we observed an increase in TBARS, PCs, MMP-2, and MMP-9, and also TIMP-1 and TIMP-2 in comparison with the control group. A positive correlation between TBARS and PCs emerged in obese subjects and persisted after dividing obese subjects according to BMI. The correlation between MMP-2 and TIMP-2 was not statistically significant, while a significant correlation was present between MMP-9 and TIMP-1. The correlations between the markers of oxidative stress (TBARS and PCs) and those of the MMP/TIMP profile indicated a more marked influence of protein oxidation on MMPs and TIMPs in comparison with TBARS. The innovative aspect of our study was the simultaneous evaluation of oxidative stress markers and MMP/TIMP profile in adult obese subjects. We observed significant alterations and correlations that may negatively influence the clinical course of the disease.

scholarly journals Relation between Gastric Cancer and Protein Oxidation, DNA Damage, and Lipid Peroxidation

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Yongsheng Ma ◽  
Lin Zhang ◽  
Shengzhong Rong ◽  
Hongyan Qu ◽  
Yannan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastric Cancer ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Protein Oxidation ◽  
Antioxidant Defense System ◽  
Protein Carbonyl ◽  
Treatment And Prevention ◽  
Healthy Control ◽  
The Relationship

Objects.The aim of this study is to evaluate protein oxidation, DNA damage, and lipid peroxidation in patients with gastric cancer and to investigate the relationship between oxidative stress and gastric cancer.Methods. We investigated changes in serum protein carbonyl (PC), advanced oxidation protein products (AOPP), and 3-nitrotyrosine (3-NT) levels, as indicators of protein oxidation, serum 8-hydroxydeoxyguanosine (8-OHdG), as a biomarker of DNA damage, and malondialdehyde (MDA), conjugated diene (CD), 4-hydroxynonenal (4-HNE), and 8-ISO-prostaglandinF2α(8-PGF) in serum, as lipid peroxidation markers in gastric cancer (GC) patients and healthy control.Results. Compared with control, a statistically significant higher values of 8-OHdG, PC, AOPP, and 3-NT were observed in the GC patients (P<0.05). The products of lipid peroxidation, MDA, CD, 4-HNE, and 8-PGF, were significantly lower in the GC patients compared to those of control (P<0.05). In addition, the products of oxidative stress were similar between the Helicobacter pylori positive and the negative subgroups of GC patients.Conclusions. GC patients were characterized by increased protein oxidation and DNA damage, and decreased lipid peroxidation. Assessment of oxidative stress and augmentation of the antioxidant defense system may be important for the treatment and prevention of gastric carcinogenesis.

Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise

1997 ◽  
Vol 83 (1) ◽  
pp. 189-195 ◽  
Author(s):  
Chandan K. Sen ◽  
Mustafa Atalay ◽  
Jyrki Ågren ◽  
David E. Laaksonen ◽  
Sashwati Roy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Vitamin E ◽  
Physical Exercise ◽  
Fish Oil ◽  
Protein Oxidation ◽  
Protein Carbonyl ◽  
Oxidative Protein Damage ◽  
Exercise Induced ◽  
Vitamin E Supplementation

Sen, Chandan K., Mustafa Atalay, Jyrki Ågren, David E. Laaksonen, Sashwati Roy, and Osmo Hänninen. Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise. J. Appl. Physiol.83(1): 189–195, 1997.—Fish oil supplementation and physical exercise may induce oxidative stress. We tested the effects of 8 wk of α-tocopherol (vitamin E) and fish oil (FO) supplementation on resting and exercise-induced oxidative stress. Rats ( n = 80) were divided into groups supplemented with FO, FO and vitamin E (FOVE), soy oil (SO), and SO and vitamin E (SOVE), and for FOVE and SOVE they were divided into corresponding exercise groups (FOVE-Ex and SOVE-Ex). Lipid peroxidation [thiobarbituric acid-reacting substances (TBARS)] was 33% higher in FO compared with SO in the liver, but oxidative protein damage (carbonyl levels) remained similar in both liver and red gastrocnemius muscle (RG). Vitamin E supplementation, compared with FO and SO, markedly decreased liver and RG TBARS, but liver TBARS remained 32% higher in FOVE vs. SOVE. Vitamin E also markedly decreased liver and RG protein carbonyl levels, although levels in FOVE and SOVE were similar. Exercise increased liver and RG TBARS and RG protein carbonyl levels markedly, with similar levels in FOVE-Ex and SOVE-Ex. FO increased lipid peroxidation but not protein oxidation in a tissue-specific manner. Vitamin E markedly decreased lipid peroxidation and protein oxidation in both FOVE and SOVE, although liver lipid peroxidation remained higher in FOVE. Despite higher levels of hepatic lipid peroxidation at rest in FOVE compared with SOVE, liver appeared to be relatively less susceptible to exercise-induced oxidative stress in FOVE.

Diallyl trisulfide ameliorates arsenic-induced hepatotoxicity by abrogation of oxidative stress, inflammation, and apoptosis in rats

2014 ◽  
Vol 34 (5) ◽  
pp. 506-525 ◽  
Author(s):  
NC Sumedha ◽  
S Miltonprabu
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Oxidation ◽  
Structural Changes ◽  
Histopathological Examination ◽  
Thiobarbituric Acid ◽  
Hepatic Function ◽  
Protein Carbonyl ◽  
Thiobarbituric Acid Reactive Substance ◽  
Diallyl Trisulfide

The present study investigates the possible ameliorative effects of diallyl trisulfide (DATS) against arsenic (As)-induced hepatotoxicity and oxidative stress in rats. The four experimental groups evaluated include: (1) vehicle control; (2) As (5 mg/kg/day); (3) DATS (80 mg/kg/day) + As; and (4) DATS. Induction of As in rats caused severe hepatotoxicity as evidenced by an elevation of serum aspartate aminotransferase and alanine aminotransferase activities and increased total bilirubin concentration, indicating hepatic function abnormalities. Histopathological examination revealed various structural changes in the liver, characterized by hepatocyte degeneration/necrosis, congestion, sinusoidal dilatation, vacuolation, and inflammatory cell infiltration. The significant decrease in reduced glutathione content, catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase activities and the significant increase in lipid peroxidation (thiobarbituric acid reactive substance) and protein oxidation (protein carbonyl) contents indicated that As-induced hepatotoxicity was mediated through oxidative stress. As intoxication also elevated the levels of Cas-3 and nitric oxide and increased the expression of nuclear factor-κB p65 in the liver. In contrast, DATS pretreatment significantly improved As-induced serum biochemical, immunohistochemical, and histopathological alterations reflecting hepatic dysfunction. These results may contribute to a better understanding of the hepatoprotective role of DATS, emphasizing the influence of this garlic trisulfide in the diet for human health, possibly preventing the hepatic injury associated with As intoxication, presumably due to its ability to inhibit lipid peroxidation, protein oxidation, and restoration of antioxidant status.

scholarly journals Antioxidants, lysosomes and elements status during the life cycle of sea trout Salmo trutta m. trutta L.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Natalia Kurhaluk ◽  
Halyna Tkachenko
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Muscle Tissue ◽  
Salmo Trutta ◽  
Protein Carbonyl ◽  
Oxidative Modification ◽  
Oxidative Stress Biomarkers ◽  
Development Stages ◽  
Stress Biomarkers ◽  
Element Contents

AbstractThe aim of our study was to elucidate the effects of both development stages (parr, smolt, adult, spawner), and kelt as a survival form and sex (male, female) on the functional stability of the lysosomal complex, biomarkers of oxidative stress, and element contents in the muscle tissue of the sea trout (Salmo trutta m. trutta L.) sampled in the Pomerania region (northern Poland). We have evaluated the maximal activities of lysosomal enzymes (alanyl aminopeptidase, leucyl aminopeptidase, β-N-acetylglucosaminidase, and acid phosphatase), lipid peroxidation level, and protein carbonyl derivatives as indices of muscle tissue degradation. The relationship between lysosomal activity and oxidative stress biomarkers estimated by the lipid peroxidation level and protein carbonyl derivatives was also assessed, as well as the relationships between element levels and oxidative stress biomarkers. Trends of the main effects (i.e., the development stages and sex alone, the interaction of the sex and development stage simultaneously) on oxidative stress biomarkers, lysosomal functioning, and element contents in the muscle tissue were evaluated. The study has shown sex-related relationships between the pro- and antioxidant balance and the tissue type in the adult stage as well as modifications in the lysosomal functioning induced by long-term environmental stress associated with changing the habitats from freshwater to seawater and intense migrations. The highest level of toxic products generated in oxidative reactions and oxidative modification of proteins was noted in both the spawner stage and the kelt form. The holistic model of analysis of all parameters of antioxidant defense in all development stages and sex demonstrated the following dependencies for the level of lipid peroxidation, oxidative modification of proteins, lysosomal activities, and element contents: TBARS > OMP KD > OMP AD > TAC, AcP > NAG > LAP > AAP and Cu > Fe > Ca > Mn > Zn > Mg, respectively.

scholarly journals Susceptibility to oxidative stress, insulin resistance, and insulin secretory response in the development of diabetes from obesity

2007 ◽  
Vol 64 (6) ◽  
pp. 391-397 ◽  
Author(s):  
Radivoj Kocic ◽  
Dusica Pavlovic ◽  
Gordana Kocic ◽  
Milica Pesic
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Lipid Peroxidation ◽  
Insulin Sensitivity ◽  
Healthy Subjects ◽  
Critical Role ◽  
Secretory Response ◽  
Diabetic Patients ◽  
Apparent Difference ◽  
Insulin Secretory Response

Background/Aim. Oxidative stress plays a critical role in the pathogenesis of various diseases. Recent reports indicate that obesity may induce systemic oxidative stress. The aim of the study was to potentiate oxidative stress as a factor which may aggravate peripheral insulin sensitivity and insulinsecretory response in obesity in this way to potentiate development of diabetes. The aim of the study was also to establish whether insulin-secretory response after glucagonstimulated insulin secretion is susceptible to prooxidant/ antioxidant homeostasis status, as well as to determine the extent of these changes. Methods. A mathematical model of glucose/insulin interactions and C-peptide was used to indicate the degree of insulin resistance and to assess their possible relationship with altered antioxidant/prooxidant homeostasis. The study included 24 obese healthy and 16 obese newly diagnozed non-insulin dependent diabetic patients (NIDDM) as well as 20 control healthy subjects, matched in age. Results. Total plasma antioxidative capacity, erythrocyte and plasma reduced glutathione level were significantly decreased in obese diabetic patients, but also in obese healthy subjects, compared to the values in controls. The plasma lipid peroxidation products and protein carbonyl groups were significantly higher in obese diabetics, more than in obese healthy subjects, compared to the control healthy subjects. The increase of erythrocyte lipid peroxidation at basal state was shown to be more pronounced in obese daibetics, but the apparent difference was obtained in both the obese healthy subjects and obese diabetics, compared to the control values, after exposing of erythrocytes to oxidative stress induced by H2O2. Positive correlation was found between the malondialdehyde (MDA) level and index of insulin sensitivity (FIRI). Conclusion. Increased oxidative stress together with the decreased antioxidative defence seems to contribute to decreased insulin sensitivity and impaired insulin secretory response in obese diabetics, and may be hypothesized to favour the development of diabetes during obesity.

scholarly journals Strawberry Intake Ameliorates Oxidative Stress and Decreases GABA Levels Induced by High-Fat Diet in Frontal Cortex of Rats

Antioxidants ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 70 ◽  
Author(s):  
Cuauhtémoc Sandoval-Salazar ◽  
Cecilia Oviedo-Solís ◽  
Edmundo Lozoya-Gloria ◽  
Herlinda Aguilar-Zavala ◽  
Martha Solís-Ortiz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Frontal Cortex ◽  
Protein Oxidation ◽  
High Fat Diet ◽  
High Fat ◽  
Gaba Concentration ◽  
Obese Rats ◽  
Lipid And Protein Oxidation

It has been proposed that there is a correlation between high-fat diet (HFD), oxidative stress and decreased γ-aminobutyric acid (GABA) levels, but this has not been thoroughly demonstrated. In the present study, we determined the effects of strawberry extract intake on the oxidative stress and GABA levels in the frontal cortex (FC) of obese rats. We observed that an HFD increased lipid and protein oxidation, and decreased GABA levels. Moreover, UV-irradiated strawberry extract (UViSE) decreased lipid peroxidation but not protein oxidation, whereas non-irradiated strawberry extract (NSE) reduced protein oxidation but not lipid peroxidation. Interestingly, NSE increased GABA concentration, whereas UViSE was not as effective. In conclusion, our results suggest that an HFD increases oxidative damage in the FC, whereas strawberry extract intake may ameliorate the disturbances associated with HFD-induced oxidative damage.

scholarly journals Comparative effect of bovine buttermilk, whey, and lactoferrin on the innate immunity receptors and oxidative status of intestinal epithelial cells.

2020 ◽  
Author(s):  
Berta Buey ◽  
Andrea Bellés ◽  
Eva Latorre ◽  
Inés Abad ◽  
María Dolores Pérez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Innate Immunity ◽  
Epithelial Cells ◽  
Milk Fat ◽  
Functional Foods ◽  
Intestinal Epithelial Cells ◽  
Protein Carbonyl ◽  
Intestinal Epithelial ◽  
Milk Fat Globule

Milk contains active molecules with important functional properties as the defensive proteins; among them are the whey protein lactoferrin and proteins of the milk fat globule membrane (MFGM) present in buttermilk. The aim of this study has been to investigate the effect of lactoferrin, whey and buttermilk as modulators of intestinal innate immunity and oxidative stress on intestinal epithelial cells, to evaluate its potential use for the development of functional foods. Innate immune Toll-like receptors (TLR2, TLR4, and TLR9) mRNA expression, lipid peroxidation (MDA+4-HDA) and protein carbonyl levels were analyzed in enterocyte-like Caco-2/TC7 cells treated for 24 hours with different concentrations of lactoferrin, whey or buttermilk. None of the substances analyzed caused oxidative damage; however, whey significantly decreased the levels of lipid peroxidation. Furthermore, both lactoferrin and whey were able to reduce the oxidative stress induced by lipopolysaccharide. Respect to TLR receptors, lactoferrin, whey and buttermilk specifically altered the expression of TLR2, TLR4 and TLR9 receptors, with a strong decrease in TLR4 expression. These results suggest that lactoferrin, whey and buttermilk could be interesting potential ingredients for functional foods as they seem to modulate oxidative stress and inflammatory response induced by TLRs activation.

scholarly journals Oxidative Stress Induction by Lead in Leaves of Radish (Raphanus sativus) Seedlings

2011 ◽  
Vol 3 (4) ◽  
pp. 93-99 ◽  
Author(s):  
Nadjet BITEUR ◽  
Abdelkader AOUES ◽  
Omar KHAROUBI ◽  
Miloud SLIMANI
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Oxidation ◽  
Raphanus Sativus ◽  
Lead Concentration ◽  
Control Treatment ◽  
Enzymatic Antioxidants ◽  
Carotenoid Concentration ◽  
Hydroponic System ◽  
Physiological Processes

Oxidative stress was induced by lead acetate (Pb) in Raphanus sativus seedlings grown in a hydroponic system using sand as substrate. Thirty day old acclimated seeds were treated for 7 days with five Pb levels (0 as control, 100, 200, 500 and 1000 mg l-1). Parameters such as growth, oxidative damage markers (lipid peroxidation, protein oxidation and hydrogen peroxide contents) and enzymatic activities of catalase (CAT) and peroxidase (POD) were investigated. Lead concentration in plant tissues increased with increasing of Pb levels. Shoot fresh weight, chlorophyll and carotenoid concentration were significantly decreased at 100 mg l-1 Pb. Lipid peroxidation, protein oxidation and H2O2 levels were increased at 500 and 1000 mg l-1 Pb compared to control treatment, in shoots. Peroxidase activity showed a straight correlation with H2O2 concentration, whereas CAT activity decreased only in shoots. These changes in enzymatic and non-enzymatic antioxidants showed that the Pb exposition had a significant disturbance on Raphanus sativus plantlets and affect the biochemical and physiological processes.

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