scholarly journals Proanthocyanidins Alleviates AflatoxinB1-Induced Oxidative Stress and Apoptosis through Mitochondrial Pathway in the Bursa of Fabricius of Broilers

Toxins ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 157 ◽  
Author(s):  
Shahid Rajput ◽  
Cong Zhang ◽  
Yue Feng ◽  
Xiao Wei ◽  
Mahmoud Khalil ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Protein Expression ◽  
Basal Diet ◽  
Mitochondrial Pathway ◽  
Bursa Of Fabricius ◽  
Enzymes Activities ◽  
Study Results ◽  
Mrna And Protein Expression ◽  
Antioxidant Enzymes Activities

Aflatoxin B1 (AFB1) is a serious threat to the poultry industry. Proanthocyanidins (PCs) demonstrates a broad range of biological, pharmacological, therapeutic, and chemoprotective properties. The aim of this study was to investigate the ameliorative effects of PCs against AFB1-induced histopathology, oxidative stress, and apoptosis via the mitochondrial pathway in the bursa of Fabricius (BF) of broilers. One hundred forty-four one-day old Cobb chicks were randomly assigned into four treatment groups of six replicates (6 birds each replicate) for 28 days. Groups were fed on the following four diets; (1) Basal diet without addition of PCs or AFB1 (Control); (2) basal diet supplemented with 1 mg/kg AFB1 from contaminated corn (AFB1); (3) basal diet supplemented with 250 mg/kg PCs (PCs); and (4) basal diet supplemented with 1 mg/kg AFB1 + 250 mg/kg PCs (AFB1+ PCs). The present study results showed that antioxidant enzymes activities of total superoxide dismutase (T-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione S-transferase (GST) in AFB1 treated group were (p < 0.05) decreased, whereas malondialdehyde (MDA) contents were significantly increased in comparison with the control group. Furthermore, we found that dietary PCs treatment ameliorated AFB1-induced oxidative stress in the BF through inhibiting the accumulation of MDA content and enhancing the antioxidant enzymes activities (T-SOD, CAT, GSH-Px, and GST). Similarly, PCs markedly enhanced messenger RNA (mRNA) expression of antioxidant genes (SOD, CAT, GPx1, and GST) in comparison with AFB1 group. Moreover, histological results showed that PCs alleviated AFB1-induced apoptotic cells in the BF of broilers. In addition, both mRNA and protein expression results manifested that mitochondrial-apoptosis-associated genes (Bax, caspase-9, caspase-3, and p53 and cytochrome c) showed up-regulation, while (Bcl-2) showed down-regulation in AFB1 fed group. The supplementation of PCs to AFB1 diet significantly reversed the mRNA and protein expression of these apoptosis-associated genes, as compared to the AFB1 group. Our results demonstrated that PCs ameliorated AFB1-induced oxidative stress by modulating the antioxidant defense system and apoptosis in the BF through mitochondrial pathway in broilers.

scholarly journals Hepatic Postnatal Developmental Expression of Trace Mineral Associated Antioxidant Enzymes

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1077-1077
Author(s):  
Laura Sherlock ◽  
Kara Sjostrom ◽  
Nancy Krebs ◽  
Clyde Wright ◽  
Eva Nozik-Grayck
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Protein Expression ◽  
Developmental Regulation ◽  
Immune Surveillance ◽  
Developmental Expression ◽  
Antioxidant Defenses ◽  
Trace Mineral ◽  
Mrna And Protein Expression ◽  
Neonatal Liver

Abstract Objectives Oxidative stress is central to the etiology of many diseases of prematurity. Lower antioxidant defenses render premature infants vulnerable to oxidative damage secondary to infection and oxygen therapy. Antioxidant enzymes (AOE) increase perinatally in the blood and lungs. Many AOE require a micronutrient such as selenium (Se) or zinc (Zn) to function at maximum efficacy. These trace elements are low in neonates compared to adults. The liver is an important immune surveillance organ where antioxidant defense is critical for host response. It also plays a major role in micronutrient processing. However, the developmental regulation and expression of AOE in the liver is incompletely described. We hypothesized the neonatal liver would have decreased trace mineral associated AOE. Methods C57BL/6mice were sacrificed at P0, P7, P21 and 8–12 weeks. mRNA and protein expression of key AOE (SOD1, SOD2, SOD3, Gpx1, Gpx4, Msrb1, TrxR1) and factors for Se processing (Sephs2/Sps2, Scly, Pstk) were measured by qPCR and Western blot. Results Hepatic mRNA for selenoenzymes Gpx1 and Msrb1 were developmentally regulated, low at P0 and increased by adult (P &lt; 0.05, n = 5–6). Gpx1 protein increased 7–8-fold and Msrb1 protein increased 6-fold from P0 to adult (P &lt; 0.0001, n = 4). Gene expression of Zn related SOD1 and Mn SOD2 increased postnatally, low at P0 and increased in adult (P &lt; 0.01 n = 5–6). Protein expression for each increased 1.5 and 3-fold from P0 to adult respectively (P &lt; 0.001, n = 4) The mRNA and protein expression for Gpx4, TrxR1 and SOD3 remained constant postnatally. As the greatest increase was observed in selenoenzymes, factors for Se processing were evaluated. Sephs2, Scly and Pstk mRNA increased from P0 compared to P21 and adult mice (P &lt; 0.05, n = 4–6). Protein expression for Pstk and Scly was highest at P21 and protein for Sps2 increased postnatally (P &lt; 0.01, n = 4). Conclusions The liver experiences a postnatal increase in essential trace mineral associated AOE. Additionally, the hepatic machinery for Se processing is low in neonatal mice. We speculate that the neonatal liver is vulnerable to oxidative stress secondary to low AOE defense. We also speculate states that decreased neonatal micronutrient status may further impair the hepatic redox state. Funding Sources CCTSI Child Maternal Health Mentored Grant (L.S).

scholarly journals Fresh Bitter Melon Fruit (Momordica charantia) Attenuated Oxidative Stress, Fibrosis and Renal Injury in Carbon Tetrachloride Treated Rats

2018 ◽  
Vol 16 (2) ◽  
pp. 205-214 ◽  
Author(s):  
Md Abu Taher Sagor ◽  
Hasan Mahmud Reza ◽  
Nabila Tabassum ◽  
Md Moshfequr Rahman ◽  
Md Ashraful Alam
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Carbon Tetrachloride ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Immune Cell ◽  
Enzymes Activities ◽  
Antioxidant Enzymes Activities ◽  
Stage Renal Disease ◽  
End Stage

Chemical or drug-induced kidney damage is increasing every year and the end-stage renal disease is becoming a burden for health care system of many countries. Oxidative stress may be a crucial pathway for the development of end-stage renal disease. Thus, natural antioxidant or plant-based therapy would be a better alternative to protect renal function against chemical-induced renal damage. To determine these aspects we evaluated renoprotective effects of M. charantia in carbon tetrachloride administered rats. A 10% w/w mixture of fresh fruits of M. charantia was given with the chow food every day to CCl4 treated rats. After fourteen days, all animals were sacrificed and the kidneys were examined to observe the possible protective effects of M. charantia against CCl4 induced toxicity. The CCl4 treated rats showed increased oxidative stress parameters and decreased antioxidant enzymes activities. Supplementation of 10% w/w M. charantia fruits in CCl4 administered rats prevented the oxidative stress and restored the antioxidant enzymes activities. M. charantia fruits supplementation also prevented the rise of uric acid and creatinine concentration in plasma of CCl4 treated rats. Furthermore, histological studies showed that supplementation of 10% w/w M. charantia fruits prevented the collagen deposition, immune cell migration and iron deposition in kidney sections of CCl4 treated rats. The results of this study revealed that the fruits of M. charantia may protect oxidative stress-mediated damage in kidneys due to CCl4 administration, which is mediated probably via the restoration of anti-oxidant enzyme functions.Dhaka Univ. J. Pharm. Sci. 16(2): 205-214, 2017 (December)

P–086 High level of sperm DNA breaks in infertile men with varicocele: its association with sperm cells death, seminal oxidative stress, and spermatic parameters

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
O Ammar ◽  
M Mehdi
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Dna Fragmentation ◽  
Semen Parameters ◽  
Dna Breaks ◽  
Enzymes Activities ◽  
Sperm Dna ◽  
Antioxidant Enzymes Activities ◽  
High Level ◽  
And Oxidative Stress

Abstract Study question Our objectives were to determine the extent of nuclear sperm injury in varicocele patients with and without altered spermatic parameters and to investigate its relationship with apoptosis and oxidative stress. Summary answer Oxidative stress (OS) in the varicocele patients may play a role in the etiology of nuclear sperm DNA damage associated with apoptosis. What is known already Varicocele is associated with high level of DNA Breaks. Study design, size, duration Ejaculated sperm samples from 51 patients diagnosed with varicocele and 29 fertile men were examined. According to the guidelines, the patient’s sperm samples were classified into varicocele with normal semen parameters (n = 11) and varicocele with abnormal semen parameters (n = 40). Participants/materials, setting, methods Sperm DNA breaks was assessed using terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The proportion of both viable and dead spermatozoa with externalized phosphatidylserine was detected by the bivariate annexin V cy3/6-CFDA staining method. Seminal malondialdehyde (MDA) amounts and antioxidant enzymes activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured spectrophotometrically. Main results and the role of chance Sperm DNA Breaks, viable spermatozoa with externalized PS, and MDA levels were significantly higher in studied subgroups of patients with varicocele, either with normal or with abnormal semen parameters than controls. The seminal antioxidant enzymes activities were significantly reduced in both subgroups of patients with varicocele compared to the controls. The percentage of spermatozoa with fragmented DNA was positively correlated to the MDA level as well as the proportion of viable spermatozoa with externalized PS. However, the decreased seminal antioxidant status was negatively correlated with the increased proportion of sperm DNA fragmentation and apoptotic spermatozoa. Limitations, reasons for caution We suggest further comparative studies connecting the varicocele patients with and without altered spermatic parameters representing high level of DNA fragmentation with more apoptotic and oxidative stress markers. Wider implications of the findings: This study reveals that impaired seminal antioxidant profile and increased seminal level of lipid peroxidation may be involved in the pathophysiological mechanisms of cell death-mediated DNA breaks in patients with varicocele. Trial registration number Not applicable

Amelioration of Benzo[a]pyrene-induced oxidative stress and pulmonary toxicity by Naringenin in Wistar rats: A plausible role of COX-2 and NF-κB

2016 ◽  
Vol 36 (4) ◽  
pp. 349-364 ◽  
Author(s):  
R Ali ◽  
A Shahid ◽  
N Ali ◽  
SK Hasan ◽  
F Majed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Pulmonary Toxicity ◽  
Radical Scavenging ◽  
Protective Agent ◽  
Enzymes Activities ◽  
Cell Counts ◽  
Antioxidant Enzymes Activities ◽  
Cox 2

Naringenin is a naturally occurring flavanones and has been found to exhibit free radical scavenging, enzyme inhibition, antioxidants, anti-inflammatory, and anticancer activities. Present study was designed to evaluate the protective role of naringenin against benzo[a]pyrene (B[a]P)-induced oxidative stress and pulmonary toxicity. Rats were treated with naringenin at a dose of 100 mg/kg body weight (b. wt.), by oral gavage. B[a]P in a single dose of 50 mg/kg b. wt. was given intraperitoneally. Total protein, total cell counts, lactate dehydrogenase, lipid peroxidation, reduced glutathione, antioxidant enzymes activities, lung histology and expression of nuclear factor kappa B (NF-κB), and cyclo-oxygenase-2 (COX-2) was assessed to evaluate protective effects of naringenin. Histopathological and immunohistochemical studies were also carried out to observe lung toxicity and inflammation. B[a]P administration enhanced the levels of lung injury markers and reduced antioxidant enzymes activities. Naringenin treatment attenuated the levels of oxidative stress by restoring antioxidant enzymes, further improved lung histological damage and significant decrease in inflammatory responses. Naringenin also effectively decreased the expression of NF-κB, and COX-2 induced by B[a]P. These findings suggest that naringenin supplementation is beneficial in maintaining the integrity of alveoli and the epithelium that may be used as a protective agent in B[a]P-induced oxidative stress and lung damage. However, further studies are warranted to elucidate the potential mechanism of action of naringenin.

scholarly journals The Relationship between Coenzyme Q10, Oxidative Stress, and Antioxidant Enzymes Activities and Coronary Artery Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Bor-Jen Lee ◽  
Yi-Chin Lin ◽  
Yi-Chia Huang ◽  
Ya-Wen Ko ◽  
Simon Hsia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Antioxidant Enzymes ◽  
Coronary Artery ◽  
Coenzyme Q10 ◽  
Control Group ◽  
Enzymes Activities ◽  
Antioxidant Enzymes Activities ◽  
Artery Disease ◽  
The Relationship

A higher oxidative stress may contribute to the pathogenesis of coronary artery disease (CAD). The purpose of this study was to investigate the relationship between coenzyme Q10 concentration and lipid peroxidation, antioxidant enzymes activities and the risk of CAD. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery were assigned to the case group (n=51). The control group (n=102) comprised healthy individuals with normal blood biochemical values. The plasma coenzyme Q10, malondialdehyde (MDA) and antioxidant enzymes activities (catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx)) were measured. Subjects with CAD had significant lower plasma coenzyme Q10, CAT and GPx activities and higher MDA and SOD levels compared to those of the control group. The plasma coenzyme Q10 was positively correlated with CAT and GPx activities and negatively correlated with MDA and SOD. However, the correlations were not significant after adjusting for the potential confounders of CAD with the exception of SOD. A higher level of plasma coenzyme Q10 (≥0.52 μmol/L) was significantly associated with reducing the risk of CAD. Our results support the potential cardioprotective impact of coenzyme Q10.

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