Toxic Effect of Lead Nitrate on Lipid Peroxidation and Protein Carbonyl Content in the Muscle of Freshwater Fish Channa striatus (Bloch, 1793)

2017 ◽  
Vol 5 (5) ◽  
pp. 828-832 ◽  
Author(s):  
Shivani Sharma ◽  
Author(s):  
Archismaan Ghosh Sutapa Mukherjee ◽  
Madhumita Roy

Presence of carcinogens, like Polycyclic Aromatic Hydrocarbons (PAH), in the form of cigarette smoke, vehicular emission and industrial emissions in our immediate surroundings is a potent health hazard. Arsenic, a carcinogenic metalloid, omnipresent in the environment, can act as co-carcinogen, where it enhances the carcinogenicity of other carcinogens. In the present study, the co-carcinogenic effect of Arsenic has been investigated, upon the 7,12-dimethylbenz[a]-anthracene (DMBA), a PAH, induced skin cancer model, in Swiss albino mice. Histological analysis revealed earlier development of invasive carcinoma in the DMBA and arsenic treated group in comparison to the DMBA treated mice alone. To understand this phenomena, ROS generation, DNA damage, lipid peroxidation, protein carbonyl content, total antioxidant capacity and activity of pro-inflammatory cytokines (TNF-α, IL6, IL17a, IL22) and their downstream modulators (NF-κB) was assessed. The results suggested that arsenic in the presence of DMBA induced higher ROS generation, greater DNA damage, elevated lipid peroxidation, increased protein carbonyl content, upregulated activity of pro-inflammatory cytokines and their downstream regulators as well as down regulated the total antioxidant capacity in comparison to DMBA alone. These findings hint at the co-carcinogenic potential of arsenic, as it significantly enhances the carcinogenicity of DMBA and hastens carcinogenesis.


2020 ◽  
Vol 70 (2) ◽  
pp. 227-237
Author(s):  
Eda Güneş

Abstract The aim of the this study was to evaluate the effects of fresh, dried and freeze-dried Centaurea depressa M. Bieb. (Asteraceae) on the oxidant and antioxidant status of the model organism D. melanogaster Meigen (Diptera: Drosophilidae) experimentally. The study was carried out from 2016 to 2019, and plant leaf extracts (0-50 mg/l) were added to insect standard artificial diets. The total protein, protein carbonyl content and glutathione-S-transferase, superoxide dismutase and catalase activities were quantified at the insect’s third larval stage. Our data showed that protein carbonyl content varied from 2.70 nmol/mg protein in the control group to 59.11 nmol/mg protein in the group fed with fresh leaf extract signifying induction of oxidative stress. All extracts increased the levels of all antioxidant enzymes and decreased the amounts of total protein. Meanwhile, the group fed with the freeze-dried extract showed no significant difference in the levels of total protein and protein carbonyl content except at the 50 mg/l concentration of the extract. Moreover, this group had superoxide dismutase and catalase activities 4 to 5 times higher than in the control group. In conclusion, induction of oxidative stress indicates that the fresh form of C. depressa leaves may have potential as a natural pesticide, whereas induction of endogenous antioxidant enzymes by the freeze-dried extract suggest its potential as an antioxidant.


Author(s):  
Pullaiah P. ◽  
Suchitra M. M. ◽  
Siddhartha Kumar B.

Background: Oxidative stress (OS) has an important role in the pathogenesis and progression of rheumatoid arthritis (RA). OS causes protein modification, thereby impairing the biological functions of the protein. This study was conducted to assess the oxidatively modified protein as protein carbonyl content and the antioxidant status as protein thiols, and to study the association between protein carbonyls and protein thiols in RA.Methods: Newly diagnosed RA patients who were not taking any disease modifying anti-rheumatic drugs were included into the study group (n=45) along with age and sex matched healthy controls (n=45). Serum protein carbonyl content and protein thiols were estimated.Results: Elevated protein carbonyl content and decreased protein thiol levels (p<0.001) were observed in RA. A significant negative correlation was observed between protein carbonyl content and protein thiol levels (p<0.001).Conclusions: Oxidative stress in RA is evidenced by enhanced protein oxidation and decreased antioxidant protein thiol levels. Decreased protein thiols may also reflect protein modifications leading to compromise in the antioxidant properties. This oxidant and antioxidant imbalance needs to be addressed by therapeutic interventions to prevent disease progression.


2012 ◽  
Vol 1 (3) ◽  
pp. 200 ◽  
Author(s):  
Sarawut Kumphune ◽  
Titiporn Mekrungruangwong ◽  
Porrnthanate Seenak ◽  
Saowanee Luangaram ◽  
Tomon Thongsri

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 3319-3319
Author(s):  
Clara Lo ◽  
Bing Zhang ◽  
Kristina Cusmano-Ozog ◽  
Wendy Wong ◽  
Michael Jeng ◽  
...  

Abstract Abstract 3319 Background: An unpredictable subset of patients (∼20–30%) with pediatric immune thrombocytopenia (ITP) progress to chronic ITP; this increases the risk of morbidity and mortality from bleeding, long-term immunomodulation, and/or splenectomy. Furthermore, treatments such as chronic steroid therapy often result in intolerable side effects, raising the need for targeted therapies. We previously tested a novel list of genes that might predict progression to chronic ITP (Zhang et al Blood 2011). Oxidative stress (OS)-related pathways were among those most significantly perturbed in chronic ITP. For further evaluation of the role of OS in ITP, we measured glutathione as a marker of redox capacity and protein carbonyl content as a marker of oxidative cell damage. Methods: Pediatric patients with primary ITP were included, with exclusion of subjects with secondary thrombocytopenia, other autoimmune disorders (ie, lupus), or other chronic illnesses. Healthy pediatric volunteers were recruited as controls. Patients had blood draws within 1 month from ITP diagnosis. Reduced (GSH) to oxidized (GSSG) glutathione ratios were measured from whole blood by tandem mass-spectrometry. Protein carbonyl content (PCC) levels were measured from platelet-rich plasma by enzyme-linked immunosorbent assay (ELISA). Subjects were followed up to 15 months from diagnosis and monitored for disease resolution or progression. Chronic ITP was defined as thrombocytopenia (platelets <100,000/μL) lasting at least 12 months from diagnosis (Rodegheiro et al Blood 2009). Acute ITP was defined as thrombocytopenia resolving within 12 months from diagnosis. Statistical significance was defined as p<0.05. Results: Between July 2009 and December 2011, 67 pediatric patients with ITP were recruited. Thirty-four patients had acute ITP, and 33 patients progressed to chronic ITP. The median age of patients was 7 years (range 18 months – 17 years). Sixty-three percent were female, 37% were male. Twenty-four pediatric controls were also recruited (46% female, 54% male). The median age of controls was 8 years (range 5 years – 17 years). Patients with ITP had significantly lower GSH:GSSG ratios compared to controls, and patients with chronic ITP had lower GSH:GSSG ratios compared to those with acute ITP (Figure 1). Furthermore, patients with ITP had significantly higher PCC levels compared to controls (Figure 2). Conclusions: This data provides further evidence for a role of oxidative stress (OS) in the pathophysiology of ITP. Furthermore, decreased redox capacity, as evidenced by the decreased glutathione ratios, may be associated with progression to chronic ITP. Reactive oxidative species (ROS) may be important in the pathogenesis of autoimmunity in ITP; oxidatively altered cellular by-products induce pathogenic antibodies and become immunogenic. This also raises a potential anti-oxidant mechanism of therapy, which may play a greater role in chronic ITP treatment. Increased understanding of OS in pediatric ITP may reveal markers of disease progression, highlighting those at greatest risk for chronic ITP and creating a role for targeted therapy. Disclosures: No relevant conflicts of interest to declare.


2010 ◽  
Vol 30 (7) ◽  
pp. 616-623 ◽  
Author(s):  
Premila Abraham ◽  
Bina Isaac

Nephrotoxicity is one of the adverse side effects of cyclophosphamide (CP) chemotherapy. In a recent study, we have demonstrated that oxidative stress and glutathione depletion play important roles in CP-induced renal damage. The aim of the study was to verify whether glutamine, the precursor for glutathione synthesis, prevents CP-induced oxidative stress and renal damage using a rat model. Adult male rats were administered a single dose of 150 mg/ kg body weight of CP intraperitoneally. The glutamine-pretreated rats were administered 1 gm/kg body weight of glutamine orally 2 h before the administration of CP. Vehicle/glutaminetreated rats served as controls. All the rats were killed 16 h after the dose of CP/vehicle. The kidneys were removed and used for light microscopic and biochemical studies. The markers of oxidative stress including malondialdehyde content, protein carbonyl content, protein thiol, reduced glutathione and myeloperoxidase activity, a marker of neutrophil infiltration, were measured in kidney homogenates. CP treatment-induced damage to kidney involved the glomeruli and the tubules. Pretreatment with glutamine reduced CP-induced glutathione depletion and increased myeloperoxidase activity. However, it did not prevent CP-induced lipid peroxidation, protein carbonylation and renal damage. The results of the present study suggest that glutamine pretreatment does not prevent CP-induced lipid peroxidation and renal damage, although it prevents CP-induced glutathione depletion and neutrophil infiltration significantly. It is suggested that mechanisms other than oxidative stress may also be involved and/or oxidative stress may be consequence and not the cause of CP induced renal damage.


2006 ◽  
Vol 164 ◽  
pp. S136
Author(s):  
Vügar Aliyev ◽  
Banuçiçek Yücesan ◽  
Şebnem Ş. Çeçen ◽  
Ayşe Karakuş ◽  
Serap Yalçın ◽  
...  

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