Protein Carbonyl Content Levels Research Articles

Oxidative Stress, DNA Damage, Inflammation and Endothelial Dysfunction in Snakebite-Induced Acute Kidney Injury

Background Snakebite-induced acute kidney injury (SAKI) is a life-threatening complication. Despite its impact on public health, the understanding of the underlying cellular and molecular mechanisms remains limited. There is a lack of studies investigating the role of oxidative stress, oxidative deoxyribonucleic acid (DNA) damage, inflammation, and endothelial dysfunction in SAKI. This study aims to address this knowledge gap. Materials and Methods Biomarkers of oxidative stress, including oxidative DNA damage, inflammation, and endothelial dysfunction were assessed in 30 patients with SAKI and 30 healthy controls. Malondialdehyde (MDA), protein carbonyl content (PCC), advanced glycation end products (AGEs), 8-hydroxy-2’-deoxyguanosine (8-OHdG), ferric reducing ability of plasma (FRAP), high-sensitivity C-reactive protein (hs-CRP), and nitric oxide (NO) were used as biomarkers. Results We found significantly elevated levels of MDA (2.1590±0.68221 µmol/L vs 0.8769±0.2958 µmol/L, p = <0.001), PCC (0.0905±0.040 nmol/L vs 0.0501±0.024 nmol/L, p = <0.001) and 8-OHdG (47.0757±37.09105 ng/mL vs 18.8450±9.31479 ng/mL, p = <0.001) in SAKI patients compared to controls, indicating increased oxidative damage to lipids, proteins, and DNA respectively. Although AGEs showed higher levels in SAKI patients, the difference was not significant. FRAP levels were significantly reduced [0.214 (0.051-0.489) mmol/L vs 0.470 (0.136-0.564) mmol/L, p = 0.024], indicating compromised antioxidant capacity. Significantly elevated levels of hs-CRP [40.18 (16.96-77.56) mg/L vs 1.44 (0.5-4.45) mg/L, p = <0.001] and NO [25.59 (22.75-28.43) µmol/L vs 14.218 (11.37-16.35) µmol/L, p = <0.001] confirmed the presence of inflammation and endothelial dysfunction in these patients. Conclusion Our study demonstrated oxidative stress, including oxidative DNA damage, inflammation, and endothelial dysfunction, in SAKI patients. Understanding these intricate mechanisms could lead to the development of novel diagnostic tools and therapeutic strategies.

Oxidative-Stress and Hematological Alterations Induced by the Egyptian Naja nubiae Venom in Rats

Background: Snake venoms have been the subject of intense studies to understand the mechanisms involved in toxicity. Limited information is available regarding the Egyptian Spitting Cobra’s oxidative stress and hematological profile (Naja nubiae). Objectives: The present study aimed to evaluate the oxidative stress produced by the venom of N. nubiae and determine its hematotoxic effects in rats. Methods: The adult male Albino rats (N=30) were subcutaneously (SC) injected with a physiological saline solution in the control group. The SC injection of snake venom in groups 2 and 3 was 1/4 and 1/2 of the LD50 (0.32 mg/kg and 0.65 mg/kg body weight, respectively). Blood samples were collected at 30, 120, and 360 minutes post-injection for biochemical and hematological assays in both control and treated groups. Levels of oxidative stress biomarkers, including lipid peroxidation (LPO), protein carbonyl content (PCC), and nitric oxide (NO) were estimated. Antioxidants agents comprising glutathione (GSH) level, activities of superoxide dismutase (SOD), and catalase (CAT) were also evaluated. Results: The results showed that the effects of snake venom on blood cells are dose-dependent. Furthermore, significant alterations (P≤0.05) were observed in the hemoglobin (Hb) concentration, packed cell volume (PCV), and the number of red blood cells (RBCs) in response to a low dose of venom at the 30-minute time. In contrast to the control group, the venom induced a substantial elevation in LPO, NO, and PCC levels, indicating a disturbance in redox equilibrium. Additionally, significant reductions were detected in the GSH levels as well as SOD and CAT activities in all treated groups. Conclusion: Overall, the cytotoxicity’s potential to induce oxidative stress may reduce its antioxidant systems, leading to redox disturbance and hematological alteration.

Dietary supplementation of ark clams protects gut health and modifies gut microbiota in d-galactose-induced aging rats.

Ark clams, a seafood abundant in various nutrients, are widely consumed worldwide. This study aimed to investigate the protective benefits of two common ark clams in Korea, Scapharca subcrenata (SS) and Tegillarca granosa (TG), on gut health in d-galactose (d-gal)-induced aging rats. Thirty-two Wistar rats (11 weeks old) were randomly allocated into four groups: a CON group (normal diet + saline intraperitoneal (i.p.) injection), a CD group (normal diet + d-gal i.p. injection), an SS group (normal diet with 5% SS supplementation + d-gal i.p. injection), and a TG group (normal diet with 5% TG supplementation + d-gal i.p. injection). After 12 weeks of treatment, histopathological results showed that gut barrier damage was alleviated in rats of the SS and TG groups, as evidenced by increases in mucus layer thickness and goblet cell numbers. Meanwhile, the two groups supplemented with ark clams showed an evident reduction in oxidative stress biomarkers (malondialdehyde and protein carbonyl content levels in the colon) and an increase in the immune-related factor (immunoglobulin A level in the plasma) in rats. The 16S ribosomal RNA analysis revealed that SS and TG ark clams significantly increased the proliferations of Bacteroidetes at the phylum level and Parabacteroides at the genus level. Additionally, the levels of the three main short-chain fatty acids in the cecal contents were also significantly increased in the SS and TG groups. Our results indicated a potent preventive effect of SS and TG ark clams on d-gal-induced gut injury, suggesting that ark clams may be a promising dietary component for intervening in aging. © 2023 Society of Chemical Industry.

Does oestradiol treatment alleviate obesity-induced oxidative stress in the male liver?

The liver is an organ in which many oxidative processes occur and represents an important target of oxidative stress (OxS). Under physiological conditions of normal mitochondrial homeostasis, hepatocytes effectively remove reactive oxygen species (ROS) by enabling metabolic adaptations and through the antioxidant defence system mechanisms. However, obesity-induced lipid accumulation in the hepatocytes causes significantly elevated production of ROS, reduces oxidative capacity, and increases oxidative stress (OxS). In men, compared with premenopausal women, the development of insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) in obesity are more prevalent, where oestradiol (E2), the most potent female sex steroid, is proposed as the main culprit. Exogenous oestradiol (E2) administration exerts beneficial effects on antioxidant properties, restores total plasma antioxidant capacity and decreases biomarkers of OxS in ovariectomized animal models. Thus, we hypothesized that E2 treatment in states of obesity could have beneficial effects againstOxS in the obese male's liver. We assumed that E2 could directly affect the level of OxS by increasing the level/activity of the AOS enzymes, particularly SOD1, SOD2, GPx, and CAT, in obese males' livers. In addition, we assumed that the level of malondialdehyde (MDA) and protein carbonyl content (PCC) in obese males' livers would be reduced after E2 treatment as a result of E2 inhibitory effect on lipid peroxidation and protein oxidation, respectively. To test our hypothesis, we used the liver of a high-fat (HF) diet-fed male Wistar rats as an animal model of obesity, treated with E2 intraperitoneally (40 μg/kg). Preliminary results from this study support our hypothesis that E2 increases liver protein expression of AOS enzymes: SOD1, GPx, and CAT, in control and HF male rats compared with their respective controls. The protein level of SOD2 and CAT activity was increased in HF treated with E2 compared with non-treated HF rats. Moreover, as we expected, E2 administration significantly decreased the MDA level in both E2-treated groups compared to their controls, while the PCC level was significantly decreased in HF treated group compared with untreated HF rats. In conclusion, the preliminary results we obtained in this study indicate that E2 administration can effectively inhibit the OxS-related processes in the liver in HF diet-induced obesity by increasing AOS enzymes levels and CAT activity, and also by decreasing levels of MDA and PCC. A consequence of our hypothesis is that treatment with E2 may be an innovative way to improve obesity-related liver disease prevention and healing.

Evaluation of the antioxidant activities of green synthesized selenium nanoparticles and their conjugated polyethylene glycol (PEG) form in vivo

Uncontrolled regulation of oxidative stress and reactive oxygen species (ROS) in living organisms might lead to the development of various diseases. Selenium is an element in antioxidant selenoproteins and is used in different forms as a food supplement. Selenium nanoparticles (SeNPs) could show improved activity and less toxicity; their bioactivity, biocompatibility, and binding to targets might be augmented by phytochemicals decorating their surfaces during green synthesis using plant extracts. Herein, the study evaluated the antioxidant activity of Moringa peregrina-mediated SeNPs (MPM-SeNPs) and the PEGylated form (PEG-MPM-SeNPs) in vivo in lipopolysaccharide (LPS)-induced oxidative stress in a mice model. LPS injection caused a reduction in enzyme activity of both oxidative stress biomarkers superoxide dismutase (SOD) and catalase (CAT) with an elevation in protein carbonyl content level in blood sera and liver homogenates of treated mice. MPM-SeNPs and PEG-MPM-SeNPs significantly recovered SOD activity in both blood sera and liver homogenates, as well as enhanced the specific activity of CAT in LPS-injected mice. Moreover, they caused a reduction in the carbonyl content in blood sera. Thus, both SeNPs complexes were able to amend the oxidation-induced damage in the body and protect its organs against necrosis and dysfunction.

Association of Umbilical Cord Serum Oxidative Stress Markers, ADMA and Adiponectin with Adverse Fetal Outcomes in Hypertensive Disorders of Pregnancy

Background: Limited studies are available on fetal oxidative stress and endothelial dysfunction and their association with adverse fetal outcomes in hypertensive disorders of pregnancy (HDP). Method: Umbilical cord blood samples were collected at delivery from 134 pregnant women with HDP and 59 controls. Markers of oxidative stress, endothelial dysfunction and inflammation and adipokines were analyzed. Results were correlated with adverse fetal outcomes. Results: Malondialdehyde, total antioxidant status(TAS), ADMA and hsCRP levels were increased in late and early onset preeclampsia. Adiponectin levels were decreased in early onset preeclampsia. High ADMA levels were positively associated with preterm births and fetal mortality and high TAS, protein carbonyl content(PC), ADMA and low adiponectin levels were positively associated with low birth weight babies. Conclusion: Fetal systemic oxidative stress, endothelial dysfunction and inflammation were altered in early and late onset preeclampsia. High TAS, PC and ADMA levels and low adiponectin levels were positively associated with adverse fetal outcomes in HDP.

Sorghum Protein Extract Protects RBC from Sodium Nitrite-Induced Oxidative Stress and Exhibits Anticoagulant and Antiplatelet Activity

Oxidative stress plays a critical role in the progression of diabetes, arthritis, cancer, eryptosis, cardiovascular disease, and thrombosis. Currently, antioxidants from natural sources are in high demand due to their beneficial role in the management of said diseases. The purpose of the study was to evaluate the protective effect of sorghum protein buffer extract (SBE) on sodium nitrite-induced oxidative stress and thrombosis. Protein characterization of SBE was done using SDS-PAGE. Oxidative stress in RBC was induced using sodium nitrite (NaNO2) and the key stress markers such as lipid peroxidation (LPO), protein carbonyl content (PCC), and the level of antioxidant enzymes (SOD and CAT) were measured. The anticoagulant effect of SBE was identified by employing in-vitro plasma recalcification time, activated partial thromboplastin time (APTT), prothrombin time (PT), and in-vivo mouse tail bleeding time. SBE antiplatelet activity was examined using agonist adenosine diphosphate (ADP) and epinephrine-induced platelet aggregation. Non-toxic property of SBE was identified using in-vitro direct haemolytic, haemorrhagic, and edema forming activities using experimental mice. SBE revealed similar protein banding pattern under both reduced and non-reduced conditions on SDS-PAGE. Interestingly, SBE normalized the level of LPO, PCC, SOD, and CAT in stress-inducedRBCs. Furthermore, SBE showed anticoagulant effect in platelet rich plasma by enhancing the clotting time from the control 250 s to 610 s and bleeding time from the control 200 s to more than 500 s (p<0.01) in a dose dependent manner. In addition, SBE prolonged the clot formation process of only APTT but not PT. SBE inhibited the agonists ADP and epinephrine induced platelet aggregation. SBE did not hydrolyze RBC cells, devoid of edema and haemorrhage properties. This study demonstrates for the first time the anticoagulant, antiplatelet, and antioxidant properties of SBE. Thus, the observed results validate consumption of sorghum as good for health and well-being.

Protective Effect of Docosahexaenoic Acid on Silica Nanoparticles Induced Biochemical Alterations in Rat Testes

Human health effects associated with silica exposure have been widely discussed. Environmental and occupational exposure to silica nanoparticles (SiNPs) is inevitable, as nanomaterials have become part of our daily routine. SiNPs were found to have severe toxicity than silica micro-particles in male reproductive systems. It might be due to the factor that smaller the diameter of silica nanoparticles, the greater will be the toxicity. In the present study, 40 and 80 mg SiNPs were exposed to rats for 60 days and a group treated with docosahexaenoic acid (DHA) along with SiNPs. At the end of the exposure, rats were sacrificed by anaesthetic overdose, rat testes were removed for the biochemical investigations namely, lipid peroxide levels (LPO), protein carbonyl content (PC), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione (GSH). Results of the present study demonstrates that SiNPs intoxicated rats were found increased LPO and PC level while the antioxidant level namely SOD, CAT, GPx and GSH were found to be decreased in the testes when compared with the control rats, while DHA acclimation rats were observed insignificant changes as compared with the SiNPs treated groups. On the basis of results it may be concluded that the oxidative stress markers increased in the intoxicated rats and the DHA supplementation might have rescued the SiNPs exposure.

Polyphenolic-enriched olive leaf extract attenuated doxorubicin-induced cardiotoxicity in rats via suppression of oxidative stress and inflammation

BackgroundThe therapeutic value of doxorubicin as an effective anti-neoplastic agent is limited by its cardiotoxic side effects. We investigated the effects of ethanolic leaf extracts of olive leaf OL on cardiotoxicity as well as oxidative stress which was induced by doxorubicin (DOX) in Wistar rats. The cardiotoxicity was induced by intraperitoneally injecting a single dose of doxorubicin (10 mg kg−1) after 7 days of OL administration. OL was given by gastric gavage in 250 mg/kg, 500 mg/kg and 1000 mg/kg doses of extract for 10 days.ResultsCardiac toxicity of DOX was evidenced by histopathological changes in cardiac tissues and an increase in the activities of serum markers of heart damage (AST and CK). DOX caused oxidative stress as evidenced by the elevation of malondialdehyde, protein carbonyl content levels, and catalase activity. That stress was also accompanied by a concurrent depletion of the activity of superoxide dismutase within cardiac tissues. The cardiotoxicity and oxidative stress damages caused by DOX also coincided with an increase of myeloperoxidase activity and iNOS expression. Most of these doxorubicin-induced biochemical and histological alterations were effectively attenuated by prior administration of OL. OL combination with DOX significantly increased its cytotoxicity in HepG2 liver cancer cell line and IC50 dropped from 259.35 to 158.12 μg/ml.ConclusionOL potentiated the cytotoxicity of DOX in liver cancer cell line and may play a role in the protection against its cardiotoxicity and thus can be a useful adjuvant therapy where doxorubicin is the common liver cancer-treating drug.

Role of Quercetin in the Mitigation of Lindane Induced Toxicity in Terms of Oxidative Responses and Metabolic Status in Mice Brain

Background: The current study evaluated the protective potential of quercetin against lindane induced toxicity in mice brain. For investigation, mice were allocated into four groups; the first group was the control; the second group was administered with an oral dose of lindane (25 mg/kg bw) for 4 consecutive days; the third group was exposed to quercetin (40 mg/kg bw) and to the fourth group, quercetin was administered 1 hour prior to the exposure of lindane. Objective: Two major objectives of the study were set . The first objective was to create lesions in the brain by lindane and; the second was to evaluate the neuroprotective potential of quercetin. Methods: To study oxidative responses, the levels of thiobarbituric Acid Reactive Substances (TBARS), Protein Carbonyl Content (PCC), Reduced Glutathione (GSH), Superoxide Dismutase (SOD), Catalase (CAT), and Glutathione Peroxidase (GPx) were measured in brain homogenates. Three key steps regulating enzymes of the Tricarboxylic Acid (TCA) cycle viz citrate synthase (CS), pyruvate dehydrogenase (PDH) and fumarase were also assayed. Results: Lindane treatment significantly enhanced the levels of TBARS (P&lt;0.001),PCC (P&lt;0.001), GPx (P&lt;0.001), SOD (P&lt;0.05), PDH (P&lt;0.05) and fumarase (P&lt;0.001) in brains of mice compared to control. Meanwhile, it alleviated GSH, CAT and CS (P&lt;0.05) activity. Conclusion: Pretreatment with quercetin in lindane treated group not only restored previously altered biochemical parameters after lindane treatment and also significantly improved them, which suggests that quercetin is not only safe rather is neuroprotective against lindane intoxication.

Effect of GSH and niacin combination on protein oxidation, ER stress, glycation and aggregation in HLE cells under high glucose condition

AIM: To evaluate the effects of reduced glutathione (GSH) and niacin combination on protein oxidative stress, endoplasmic reticulum (ER) stress, glycation, and aggregation of the αβ crystalline in human lens epithelial (HLE) cells treated with high glucose levels. METHODS: HLE cells were cultured and exposed to 25 mmol/L glucose to promote high glucose conditions. Groups of cells were co-treated with three different combinations of dosages: 10 μmol/L GSH+25 μmol/L niacin (P1), 30 μmol/L GSH+25 μmol/L niacin (P2), and 100 μmol/L GSH+25 μmol/L niacin (P3). After 72h incubation, protein carbonyl content (PCC) and glucose reactive protein (GRP78) content were assessed using ELISA examinations. After two-week incubation, advanced glycation end products (AGEs) were also assessed and the expression of αβ crystalline was measured using Western blot examination. RESULTS: PCC and GRP78 levels in the co-treated groups were not significantly reduced compared to control (P&gt;0.05). In contrast, there was a significant decrease of the AGEs levels in all groups co-treated with GSH and niacin when compared with the control group (P&lt;0.05). In addition, the αβ crystalline expression increased after high dose glucose administration, but decreased in all groups co-treated with GSH and combinations of GSH and niacin. CONCLUSION: Combinations of GSH and niacin inhibit the aggregation of proteins and prevent glycation in hyperglycemic HLE cells. This study shows that this combination may play an active role in preventing diabetic cataract mainly from the AGEs pathway.

The role of reduced glutathione on oxidative stress, reticulum endoplasmic stress and glycation in human lens epithelial cell culture

Context: Cataracts are currently the main cause of blindness worldwide. This condition caused by a low concentration of reduced glutathione (GSH) in the lens. Aims: To evaluate the effect of glutathione (GSH) on the hyperglycemia-induced oxidative stress, reticulum endoplasmic stress, and glycation in human lens epithelial cells. Methods: Human lens epithelial cells were cultured under high-glucose conditions. Malondialdehyde (MDA), protein carbonyl content (PCC), glucose reactive protein (GRP), and advanced glycation end product (AGE) were measured by enzyme-linked immunosorbent assay after 72 h of incubation for MDA, PCC, GRP and after 2 weeks incubation for AGE. Results: The MDA and PCC levels increased in response to high-dose glucose administration compared to the control group. MDA and PCC levels were decreased at all GSH doses, whereas the lowest mean MDA and PCC levels were observed at GSH doses of 10 and 100 μM, respectively. GRP levels increased after high-glucose administration as compared to the control group. Additionally, the groups co-treated with 30 and 100 μM GSH showed reduced PCC. The AGE level was reduced at all doses of GSH compared to those in the control group. Conclusions: The results suggest that GSH inhibits oxidative stress, reticulum endoplasmic stress, and AGE formation, which may lead to the progression of diabetic cataract. Additionally, GSH may maintain lens transparency by acting as an antiglycation and controlling the AGE formation.

Defensive proclivity of bacoside A and bromelain against oxidative stress and AChE gene expression induced by dichlorvos in the brain of Mus musculus

The objective of current study was to evaluate the neuroprotective effects of bacoside A and bromelain against dichlorvos induced toxicity. The healthy, 6–8 weeks old male Swiss mice were administered in separate groups subacute doses of dichlorvos (40 mg/kg bw), bacoside A (5 mg/kg bw) and bromelain (70 mg/kg bw). In order to determination of oxidative stress in different groups, thiobarbituric acid reactive substances (TBARS) and protein carbonyl content (PCC) were studied in the present investigation. Moreover, for toxic manifestation at molecular level the site-specific gene amplification of acetylcholinesterase (AChE) gene was studied in the brain. Nonetheless, the protective effects of bacoside A and bromelain were also evaluated on the TBARS, PCC and AChE gene. The exposure of dichlorvos leads to significant increase in TBARS level (p < 0.01, p < 0.001) and PCC. Besides, the decline in DNA yield, expression of amplified products of AChE gene was observed in the brain of dichlorvos treated group. The bacoside A and bromelain treatments significantly decreased the level of TBARS (p < 0.05, (p < 0.01) and PCC whereas, increase in the DNA yield and expression of amplified AChE gene products were observed in the brain compared to only dichlorvos treated mice. The overall picture which emerged after critical evaluation of results indicated that the dichlorvos induced oxidative stress and alteration in AChE gene expression showed significant improvement owing to the treatments of bacoside A and bromelain. Thus, bacoside A and bromelain are very effective in alleviating neurotoxicity induced by dichlorvos.

Correlation of Glycated Haemoglobin with Protein Carbonyl Content as Biomarkers of Oxidative Stress in Type 2 Diabetes Mellitus

Introduction: Diabetes is chronic disease which is characterised by defect in insulin secretion and insulin action leading to hyperglycaemia. Aim: To detect protein carbonyl as oxidative stress marker in Type 2 Diabetes Mellitus (T2DM). Materials and Methods: The present cross-sectional study was conducted on 100 subjects (aged 40 to 70 years) out of which 50 were T2DM and 50 were normal individuals. Serum was tested for Fasting Blood Sugar (FBS) and Glycated Haemoglobin (HbA1c) and Protein Carbonyl Content (PCC). Serum PCC was measured by spectrophotometric DNPH (dinitrophenylhydrazone) method of Reznick AZ and Packer L. Results: The protein carbonyl content, Fasting blood sugar and HbA1c were observed as positively correlated in type 2 diabetes mellitus as the levels of PCC, FBS and HbA1c were raised in T2DM as compared to controls. Conclusion: Increased HbA1c may be associated with generation of oxygen free radicals in the form of protein carbonyls and decreased antioxidants in T2DM.

O tratamento com ozônio pode ser uma alternativa promissora para a osteomielite? Um estudo experimental.

Objetivo: O objetivo do presente estudo foi investigar o impacto bioquímico e histopatológico do tratamento de ozônio em modelo experimental de osteomielite em ratos.&#x0D; Métodos: Vinte e quatro ratos Sprague-Dawley machos adultos (3 meses de idade, pesando de 300 a 400 g) foram alocados randomicamente em três grupos. O grupo I (n = 8) serviu como controle. No Grupo II (n = 8), o modelo de osteomielite experimental foi induzido no fêmur e não foi aplicado nenhum tratamento. O grupo III (n = 8) recebeu tratamento com ozônio intraperitoneal por 3 semanas depois da formação de osteomielite no fêmur. Foram coletadas amostras de sangue para avaliar a capacidade antioxidante total (CAT), a concentração da proteína carbonil (PCO) e da lactato desidrogenase (LDH) no soro. As amostras do fêmur foram avaliadas por histopatologia quanto a inflamação, necrose, osteomielite e formação de abscesso.&#x0D; Resultados: Os níveis séricos de TAC foram notavelmente maiores (p &lt; 0,001), enquanto os níveis de LDH foram menores (p = 0,002) no Grupo III em comparação com o Grupo II. Nenhuma diferença significativa foi detectada entre os grupos com relação ao nível de PCO. Do mesmo modo, o Grupo III apresentou resultados histopatológicos mais favoráveis para osteomielite (p = 0,008), inflamação (p = 0,001), necrose (p = 0,022) e formação de abscesso (p = 0,022).&#x0D; Conclusão: O ozônio pode ser um tratamento adjuvante útil na osteomielite. Mais estudos com animais e com seres humanos são necessários para esclarecer e confirmar esses efeitos preventivos, compreender a fisiopatologia subjacente e estabelecer diretrizes. Nível de Evidência II; Estudo prospectivo comparativo.

Niacin Regulates Glucose Reactive Protein (GRP78), Protein Carbonyl Content (PCC) and Malondialdehyde (MDA) in the Hyperglycemic Human Lens Epithelial Cells

Introduction: Niacin is part of the chemical structure of coenzymes nicotinamide adenine nucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). Previous studies suggested that a high niacin intake could decrease the prevalence of cataracts, which may delay the onset of diabetic cataract. Aim: The aim of this study was to evaluate the effect of niacin on the hyperglycemia-induced osmotic stress and oxidative stress in human lens epithelial cells. Materials and Methods: Human lens epithelial cells were cultured in a high glucose condition. Oxidative stress markers, including malondialdehyde (MDA), protein carbonyl content (PCC) and glucose reactive protein (GRP), were measured using TBARS analysis (MDA) and ELISA (PCC and GRP) after 72 h incubation. Results: The MDA levels increased after high glucose administration relative to that in the control group (p <0.05). Further, the groups that were co-treated with niacin showed decrease in the MDA levels for all doses of niacin and the lowest mean MDA level was obtained with 100 μM niacin. There was a decrease in the PCC levels for all doses, whereas the lowest mean PCC level was observed at a 100 μM niacin dose. The GRP levels increased after high glucose administration as compared with the control group. Also, the groups that were co-treated with niacin exhibited statistically significant reduction. Conclusion: These results suggest that niacin can inhibit the osmotic stress and oxidative stress which may lead to the progression of a diabetic cataract. Also, it may maintain lens transparency by acting as a precursor for glutathione biosynthesis and an antioxidant.

Effect of Short-term Quercetin, Caloric Restriction and Combined Treatment on Age-related Oxidative Stress Markers in the Rat Cerebral Cortex.

Aging is characterized by gradual accumulation of macromolecular damage leading to progressive loss of physiological function and increased susceptibility to diverse diseases. Effective anti-aging strategies involving caloric restriction or antioxidant supplementation are receiving growing attention to attenuate macromolecular damage in age associated pathology. In the present study, we for the first time investigated the effect of quercetin, caloric restriction and combined treatment (caloric restriction with quercetin) on oxidative stress parameters, acetylcholinesterase and ATPases enzyme activities in the cerebral cortex of aged male Wistar rats. 21 months aged rats were divided into four groups (n=6-8) such as group 1-fed ad libitum (AL); group 2-quercetin supplementation of 50 mg/kg b.w/day for 45 days fed ad libitum (QUER); group 3: caloric restricted (CR) (fed 40% reduced AL for 45 days); group 4-fed 40% CR and 50 mg/kg b.w/day QUER for 45 days (CR + QUER). Group 5-three month age old rats served as young control (YOUNG). Our results demonstrate that combined treatment of caloric restriction and quercetin significantly improved the age associated decline in the activities of endogenous antioxidant enzymes [such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)] and glutathione (GSH) content and attenuated elevated levels of protein carbonyl content (PCC), lipid peroxidation, lipofuscin, reactive oxygen species (ROS), and nitric oxide (NO). Furthermore, it is also observed that combined treatment ameliorated age associated alterations in acetylcholine esterase (AChE) and adenosine triphosphatases (ATPases) such as Na+/K+-ATPase and Ca+2-ATPase (but not Mg+2- ATPase) enzyme activities. Finally, we conclude that combined treatment of caloric restriction and quercetin (but not either treatment alone) in late life is an effective anti-aging therapy to counteract the age related accumulation of oxidative macromolecular damage.

Attenuation of Diabetic Retinopathy by Momordica chochinchinensis through Inhibition of AGEs and PCO in Streptozotocin Diabetic Rats

The aim of the present study was to investigate the effect of hydroalcoholic pericarp extract of Momordica chochinchinensis (HAPMC) on diabetes, oxidative stress, protein glycation and formation of advanced glycated end products (AGE) and obtain comparison with gliclazide. Albino Wistar rats were induced for diabetes by streptozotocin and divided into five groups as vehicle control (group I), disease control (group II), standard gliclazide (Group III), group IV, and V received 150, 300 mg/kg of HAPMC respectively, for a period of 12 weeks. Blood glucose levels were estimated and Cataract progression due to hyperglycemia was monitored by slit lamp biomicroscope and fundoscope at the end of every 4 weeks, the animals were sacrificed and the biochemical pathways involved in the pathogenesis of cataract such as oxidative stress by protein content, superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and aldose reductase (AR) in lens homogenates, protein carbonyl content (PCO) and advanced glycation end products (AGEs) in both serum and lens of HAPMC treated diabetic rats were compared to diabetic rats. The HAPMC was shown to have significant (p&lt;0.05) reduction of blood glucose levels compared to STZ induced diabetic rats. Slit lamp observations indicated cataract due to hyperglycemia. Progression and maturation were delayed significantly with HAPMC treatment. Photographs of fundus shows marked thickness of retina and dilated blood vessels in diabetic rats compared to control. Normal thickness of fundus and blood vessels was observed with HAPMC treatment. A significant improvement in antioxidant enzymes as SOD, CAT, GSH levels and inhibiting AR levels, and inhibition of PCO and AGE levels in lens homogenate. The histopathology of retina reveals that HAPMC treatment showed marked amelioration of all retinal cell layers damaged with STZ induction. These results suggest that the HAPMC is effective against STZ induced cataract and is beneficial in inhibition of formation of AGEs in the progression of diabetic retinopathy due to the presence of flavonoids like rutin, quercitin and kaempiferol.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Invulnerability of bromelain against oxidative degeneration and cholinergic deficits imposed by dichlorvos in mice brains

The present study elucidates the protective potential of bromelain against dichlorvos intoxication in mice brains. Dichlorvos induces the oxidative stress by disproportionating the balance between free radicals generation and their scavenging in neurons which leads to neuronal degeneration. In this study, mice were divided into four groups-group I (control), group II (dichlorvos treated), group III (bromelain treated) and group IV (exposed to both bromelain and dichlorvos both). Dichlorvos treatment increased the levels of thiobarbituric acid reactive substances (TBARS) and protein carbonyl content (PCC) which indicate the increased oxidative stress. Meanwhile, brain endogenous antioxidants and cholinesterases level was decreased after dichlorvos exposure. Levels of TBARS and PCC decreased whereas cholinesterases level was recorded to be elevated after bromelain exposure. Bromelain offered neuroprotection by decreasing oxidative stress and augmenting cholinesterases in mice brains. This study highlights the invulnerability of bromelain against oxidative and cholinergic deficits in mice brains.

(R)-\u03b1-Lipoic acid inhibits fructose-induced myoglobin fructation and the formation of advanced glycation end products (AGEs) in vitro

BackgroundFructose-mediated protein glycation (fructation) has been linked to an increase in diabetic and cardiovascular complications due to over consumption of high-fructose containing diets in recent times. The objective of the present study is to evaluate the protective effect of (R)-α-lipoic acid (ALA) against fructose-induced myoglobin fructation and the formation of advanced glycation end products (AGEs) in vitro.MethodsThe anti-glycation activity of ALA was determined using the formation of AGEs fluorescence intensity, iron released from the heme moiety of myoglobin and the level of fructosamine. The fructation-induced myoglobin oxidation was examined using the level of protein carbonyl content and thiol group estimation.ResultsThe results showed that co-incubation of myoglobin (1 mg/mL), fructose (1 M) and ALA (1, 2 and 4 mM) significantly inhibited the formation of AGEs during the 30 day study period. ALA markedly decreased the levels of fructosamine, which is directly associated with the reduction of AGEs formation. Furthermore, ALA significantly reduced free iron release from myoglobin which is attributed to the protection of myoglobin from fructose-induced glycation. The results also demonstrated a significant protective effect of ALA on myoglobin oxidative damages, as seen from decreased protein carbonyl content and increased protein thiols.ConclusionThese findings provide new insights into the anti-glycation properties of ALA and emphasize that ALA supplementation is beneficial in the prevention of AGEs-mediated diabetic and cardiovascular complications.