scholarly journals Manganese Inhibits Indomethacin-Induced Hepatorenal Oxidative Stress in Wistar Rats

2020 ◽  
pp. 79-90
Author(s):  
Tijani Stephanie Abiola ◽  
Olori Ogaraya David ◽  
Farombi Ebenezer Olatunde
Keyword(s):  
Oxidative Stress ◽  
Density Lipoprotein ◽  
Treated Group ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Cellular Processes ◽  
Concomitant Reduction ◽  
Liver And Kidney ◽  
Glutamyl Transferase ◽  
And Oxidative Stress

Aim: Manganese (Mn) is an essential trace element in many cellular processes. However, there is dearth of literature on its influence on indomethacin-induced hepatorenal damage. Therefore, this study was conducted to investigate the effect of manganese on indomethacin-induced hepatorenal damage in rats. Methods: Rats were divided into four groups of eight rats consisting of control group, indomethacin (IND) alone (20 mg/kg), Mn alone (10 mg/kg) and co-treated group that were treated orally for 14 consecutive days. Twenty four hours after treatment, under pentobarbital anesthesia, blood was collected and liver was excised to prepare homogenate and histology staining. Liver and kidney function tests aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), lactate dehydrogenase (LDH), malate dehydrogenase (MDH), glutamine dehydrogenase (GLDH), sorbitol dehydrogenase (SDH), glucose-6-phosphate dehydrogenase (G6PD), bilirubin (BIL), urea, creatinine, cholesterol (CHOL), triglycerides (TG), low and high density lipoprotein (LDL and HDL), electrolytes and oxidative stress superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and lipid peroxidation (LPO) biomarkers were assessed. Results: The results showed that indomethacin caused hepatorenal damage in rats manifested with increase in serum hepatic and renal function biomarkers. But co-administration of IND with Mn significantly (p < 0.05) decreased the level of hepatorenal biomarkers. Additionally, co-administration of IND with Mn improved the antioxidant status with concomitant reduction of LPO and restored the integrity of the liver and kidney histologically. Conclusion: The results of this study emphasize that co-administration of IND with Mn to rats alleviated IND-induced hepatorenal toxicities and oxidative stress in rats.

scholarly journals Effect of Tannin-Rich Extract of Chasmanthera dependens on Piroxicam-induced Liver Damage in Male Wistar Rats

2021 ◽  
Vol 5 (1) ◽  
pp. 27
Author(s):  
Tijani Stephanie Abiola ◽  
Olori Ogaraya David ◽  
Farombi Ebenezer Olatunde
Keyword(s):  
Oxidative Stress ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Significant Rise ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Male Wistar Rats ◽  
Anti Inflammatory ◽  
Group 2 ◽  
Glutamyl Transferase

Background: Piroxicam is one of the nonsteroidal anti-inflammatory drugs used as antipyretic, analgesic and anti-inflammatory drug often used for the relief of nonspecific fever condition and in arthritis. This study investigated the protective potential of tannin-rich extract of Chasmanthera dependens (TRECDS) against piroxicam-induced hepatotoxicity in male Wistar rats.Materials and Methods: Thirty two rats were divided into four groups. Group 1 received normal saline and served as the control group, group 2 were given 20 mg/kg piroxicam only, while groups 3 and 4 were given 20 mg/kg piroxicam with the addition of 200 and 400 mg/kg of tannin-rich extract of Chasmanthera dependens, respectively. All rats were treated orally once daily for ten days.Results: Administration of piroxicam caused liver atrophy demonstrated by significant rise in serum alanine aminotransferase (ALT), alkaline phosphatase (ALP), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), glucose-6-phosphate dehydrogenase (G6PDH) levels of albumin (ALB), bilirubin (BIL), total cholesterol (TCHOL), triglyceride (TRIGS) and low-density lipoprotein (LDL). Piroxicam also decreased high-density lipoprotein (HDL) level, enzymatic and nonenzymatic antioxidant levels significantly (p>0.05) with attendant increase in oxidative stress indices in the liver of rats compared with control group. Histological assessment reveled severe damaged to the liver of rats. However, co-administration with TRECDS reversed these observations as evidenced in the histological results.Conclusion: The findings of this study showed that exposure of rats to piroxicam provoked damage to the liver via oxidative damage and TRECDS has the potential of ameliorating the damage.Keywords: hepatotoxicity, piroxicam, Chasmanthera dependens, oxidative stress

scholarly journals TIME COURSE STUDY OF COMBINED N-ACETYL-P-AMINOPHENOL AND DICLOPHENAC INDUCED-HEPATOTOXICITY AND OXIDATIVE STRESS IN WISTAR RATS

2021 ◽  
Vol 46 (2) ◽  
Author(s):  
O. A Dosumu ◽  
D. I. Akinloye ◽  
O. B. Onunkwor ◽  
F. C. Thomas ◽  
R. A. Adeyemo
Keyword(s):  
Oxidative Stress ◽  
Liver Damage ◽  
Wistar Rats ◽  
Time Course ◽  
Time Dependent ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Dependent Manner ◽  
Glutamyl Transferase ◽  
And Oxidative Stress

The abuse of combined acetaminophen or N-acetyl-p-aminophenol (APAP) and diclofenac (DIC) due to their analgesics, anti-inflammatory and antipyretic properties is a predominant cause of hepatotoxicity and oxidative stress. This study investigated the time-course effects of APAP, DIC and their combination on biomarkers of hepatic function and oxidative stress in rats. Forty male Wistar rats were randomly divided into four groups of 10 animals each as follows; control (distilled water), APAP only, DIC only and APAP + DIC for 4 weeks. Indices of liver damage (serum ALT, alanine aminotransferase; AST, aspartate aminotransferase; ALP, alkaline phosphatase; GGT, gamma-glutamyl transferase and bilirubin) were measured. Oxidative stress biomarkers (MDA, malondialdehyde; NO, nitric oxide; CAT, Catalase activity; SOD, superoxide dismutase activity; GSH content, reduced glutathione), GR, glutathione reductase, and GST, glutathione-S-transferase) were also determined using spectrophotometric methods. Statistical analysis was done using one-way ANOVA with p < 0.05 considered significant. Acetaminophen and diclofenac caused marked liver damage as noted by time-dependent significant (p < 0.05) increased activities of serum ALT, AST, ALP, GGT, and bilirubin levels as well as significant (p < 0.05) increase in hepatic MDA and NO levels as compared to the control group. Hepatic GSH content, SOD, CAT, GPx, GST and GR activities were decreased significantly (p < 0.05) in all acetaminophen and diclofenac-treated groups compared to normal control in a time-dependent manner. These findings suggest that prolonged administration of diclofenac, acetaminophen or their combination may induce hepatotoxicity, oxidative stress and alteration of hepatic antioxidant status in a time-dependent manner.

scholarly journals Roles of Moringa oleifera Leaf Extract in Improving the Impact of High Dietary Intake of Monosodium Glutamate-Induced Liver Toxicity, Oxidative Stress, Genotoxicity, DNA Damage, and PCNA Alterations in Male Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Tarfa Albrahim ◽  
Manal Abdulaziz Binobead
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Leaf Extract ◽  
Liver Toxicity ◽  
Monosodium Glutamate ◽  
Male Rats ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Glutamyl Transferase ◽  
The Impact

It is common for food to be made more palatable through the use of the flavour enhancer monosodium glutamate, also known as vetsin powder. The purpose of the study described in this paper was to explore how vetsin-induced hepatic toxicity, DNA fragmentation, damage, and oxidative stress modifications could be mitigated with moringa leaf extract (MLE). To that end, 40 male rats were separated into four groups: normal control, positive control or MLE, vetsin, and vetsin combined with MLE. Results indicated that, compared to the control group, the levels of serum alanine aminotransferase (ALT), aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), liver malondialdehyde (MDA), DNA damage, injury, PCNA, and P53 expressions were significantly enhanced by the administration of vetsin (P<0.05). However, the vetsin group had significantly reduced levels of albumin, globulin, total protein, liver glutathione (GSH), superoxide dismutase enzyme (SOD), catalase, and glutathione S-transferase (GST) enzyme activities (P<0.05) by comparison to control. Meanwhile, modifications in liver functions, oxidative stress, DNA damage, liver injury, and PCNA expression were alleviated when vetsin was administered alongside MLE. The authors conclude that vetsin may have many side effects and that MLE can ameliorate biochemical changes, oxidative stress, hepatic injury, PCNA, and P53 alterations induced by vetsin administration.

scholarly journals Chlorogenic and Caftaric Acids in Liver Toxicity and Oxidative Stress Induced by Methamphetamine

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Khaled M. M. Koriem ◽  
Rowan E. Soliman
Keyword(s):  
Oxidative Stress ◽  
Chlorogenic Acid ◽  
Liver Toxicity ◽  
Density Lipoprotein ◽  
Acute Hepatic Failure ◽  
Protective Role ◽  
Control Group ◽  
Albino Rats ◽  
Dietary Polyphenols ◽  
And Oxidative Stress

Methamphetamine intoxication can cause acute hepatic failure. Chlorogenic and caftaric acids are the major dietary polyphenols present in various foods. The aim of this study was to evaluate the protective role of chlorogenic and caftaric acids in liver toxicity and oxidative stress induced by methamphetamine in rats. Thirty-two male albino rats were divided into 4 equal groups. Group 1, which was control group, was injected (i.p) with saline (1 mL/kg) twice a day over seven-day period. Groups 2, 3, and 4 were injected (i.p) with methamphetamine (10 mg/kg) twice a day over seven-day period, where groups 3 and 4 were injected (i.p) with 60 mg/kg chlorogenic acid and 40 mg/kg caftaric acid, respectively, one day before methamphetamine injections. Methamphetamine increased serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, bilirubin, cholesterol, low-density lipoprotein, and triglycerides. Also, malondialdehyde in serum, liver, and brain and plasma and liver nitric oxide levels were increased while methamphetamine induced a significant decrease in serum total protein, albumin, globulin, albumin/globulin ratio, brain serotonin, norepinephrine and dopamine, blood and liver superoxide dismutase, and glutathione peroxidase levels. Chlorogenic and caftaric acids prior to methamphetamine injections restored all the above parameters to normal values. In conclusion, chlorogenic and caftaric acids before methamphetamine injections prevented liver toxicity and oxidative stress where chlorogenic acid was more effective.

Sildenafil, a phosphodiesterase-5 inhibitor, offers protection against carbon tetrachloride-induced hepatotoxicity in rat

2018 ◽  
Vol 29 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Olorunfemi R. Molehin ◽  
Anne A. Adeyanju ◽  
Stephen A. Adefegha ◽  
Oluwasanmi O. Aina ◽  
Blessing A. Afolabi ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Density Lipoprotein ◽  
Serum Levels ◽  
Selective Inhibition ◽  
Guanosine Monophosphate ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Protective Agent ◽  
Glutamyl Transferase ◽  
Phosphodiesterase 5

AbstractBackground:Elevation of phosphodiesterase-5 (PDE5) activity converts cyclic guanosine monophosphate (cGMP) to 5′-GMP, a mechanism that could be associated with drug-mediated hepatotoxicity. This study investigated whether selective inhibition of PDE5 by sildenafil could offer protection against hepatotoxicity induced by carbon tetrachloride (CCl4).Methods:CCl4(0.5 mL/kg) was administered intraperitoneally to induce hepatotoxicity. The control group received normal saline. Sildenafil (5 mg, 10 mg, and 20 mg/kg, p.o.) was administered to CCl4-treated rats.Results:CCl4significantly increased the serum levels of gamma glutamyl transferase (γ-GT), alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) and reduced total protein (TP) (p<0.05). Pretreatment with sildenafil moderately reduced ALP, AST, and ALT activities with modest increase in TP level. CCl4-induced changes in the antioxidant status of the liver were significantly improved by sildenafil, especially at the lowest dose of 5 mg/kg by elevating the levels of reduced glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and glutathione-S-transferase (GST) and preventing lipid peroxidation (p<0.05). Sildenafil did not significantly alter the total cholesterol and triglyceride levels. However, high-density lipoprotein (HDL) level was significantly increased by sildenafil (p<0.05).Conclusions:The results from this study suggest that sildenafil, when used at low doses, may be a useful pharmacological protective agent against CCl4-induced hepatotoxicity.

Effect of progesterone on phosphamidon-induced impairment of memory and oxidative stress in rats

2011 ◽  
Vol 30 (10) ◽  
pp. 1626-1634 ◽  
Author(s):  
Amit K Sharma ◽  
Swapan K Bhattacharya ◽  
Naresh Khanna ◽  
Ashok K Tripathi ◽  
Tarun Arora ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Organophosphorus Pesticides ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Control Group ◽  
Protein Thiols ◽  
Acute And Chronic Exposure ◽  
The Brain ◽  
And Oxidative Stress

Progesterone (a neurosteroid) is an important modulator of the nervous system functioning. Organophosphorus pesticides like phosphamidon have been shown to adversely affect memory and induce oxidative stress on both acute and chronic exposure. The present study was therefore designed to investigate the effects of progesterone (PROG) on phosphamidon-induced modulation of cognitive function and oxidative stress in rats. Cognitive function was assessed using step-down latency (SDL) on a passive avoidance apparatus and transfer latency (TL) on an elevated plus maze. Oxidative stress was assessed by examining the levels of thiobarbituric acid reactive species (TBARS) and non-protein thiols (NP-SH) in isolated homogenized whole brain samples. The results showed a significant reduction in SDL and prolongation of TL in the phosphamidon (1.74 mg/kg/d; p.o.) treated group at weeks 6 and 8 as compared to the control group. Two weeks treatment with PROG (15 mg/kg/d; i.p.) antagonized the effect of phosphamidon on SDL as well as TL. Phosphamidon alone produced a significant increase in the brain TBARS levels and decrease in the brain NP-SH levels. Treatment with PROG (15 mg/kg/d; i.p.) attenuated the effect of phosphamidon on oxidative stress. Together, the results showed that progesterone attenuated the cognitive dysfunction and increased oxidative stress induced by phosphamidon in the brain.

scholarly journals Protective effect of vitamin E on oxidative stress and sperm apoptosis in diabetic Mice

2019 ◽  
Vol 17 (2) ◽  
pp. 127 ◽  
Author(s):  
Khadijeh Mirzaei Khorramabadi ◽  
Ali Reza Talebi ◽  
Abolghasem Abbasi Sarcheshmeh ◽  
Aghdas Mirjalili
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Protective Effect ◽  
Sperm Morphology ◽  
Sperm Count ◽  
Treated Group ◽  
Control Group ◽  
Diabetic Mice ◽  
And Oxidative Stress ◽  
Sperm Movement

Background: Generation of free radicals and oxidative stress are a major contributorto diabetes. These factors lead to the development of diabetic testicles disorders.Objective: In this study, the protective effect of vitamin E on functional disordersassociated with diabetes induced oxidative stress in male reproductive systems hasbeen investigated.Materials and Methods: Thirty-three adult male Mice were divided into control,diabetic, and untreated diabetic groups. Streptozotocin was used to induce diabetes.In the treated group, vitamin E was given to the Mice intraperitoneally for 30 days.Then, animals were anesthetized and sacrificed. Animal testicles were isolated andhomogenized in phosphate buffer and used for measuring sperm count, motility andsurvival of sperm, MDA concentration and antioxidant capacity (TAC). Apoptosis wasalso performed with the TUNEL test.Results: The results of reduction (12.03±98.11) TAC, MDA concentration (–28.5±2.58),sperm motility (unstable sperma= 86.4±7.48), sperm count (171.51), Sperm morphology(natural morphology= 49.69±31.93) and abnormal morphology (9.77±49.7)with increased oxidative damage. These changes were statistically significant incomparison with the control group for all variables other than MDA (p= 0.05). Treatmentof vitamin E diabetic Mice improved the ability of antioxidants to prevent oxidativedamage in the testicles, restore the sperm movement, and increase the number ofnormal sperm as well as TAC. The level of apoptosis in the treated group has decreasedcompared to the untreated group.Conclusion: Vitamin E protects the reproductive system against diabetes mellitus.Therefore, it was concluded that vitamin E may be a suitable agent for protecting thesperm and testicular parameters against undesirable effects of diabetes.

scholarly journals p66Shc: A novel biomarker of tubular oxidative injury in patients with diabetic nephropathy

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Xiaoxuan Xu ◽  
Xuejing Zhu ◽  
Mingming Ma ◽  
Yachun Han ◽  
Chun Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Density Lipoprotein ◽  
Oxidative Injury ◽  
Control Group ◽  
Tubular Damage ◽  
Blood Monocytes ◽  
Class Iii ◽  
Potential Biomarker ◽  
And Oxidative Stress

Abstract Increased p66Shc expression has been associated with diabetic nephropathy (DN). However, whether p66Shc can serve as a potential biomarker for tubular oxidative injury in DN is unknown. We measured the expression of p66Shc in peripheral blood monocytes (PBMs) and renal biopsy tissues from DN patients and then analysed the relationship between p66Shc expression and the clinical characteristics of patients with DN. Patients were divided into 4 groups (class IIa, class IIb, class III and the control group). qPCR, Western blotting and immunohistochemistry were performed. The results showed that both p66Shc and p-p66Shc expression significantly increased in PBMs and kidney tissues of DN patients. Moreover, Spearman’s correlation and multiple regression analyses were carried out. A positive relationship between the p66Shc expression and oxidative stress was found. p66Shc and oxidative stress were significant predictors of the degree of tubular damage. In addition, p66Shc expression was positively correlated with the concentrations of β-NAG, UACR and 8-OHdG, low-density lipoprotein and blood glucose levels, and duration of diabetes in patients with DN from class IIa to class III. These data indicated that increased expression of p66Shc may serve as a therapeutic target and a novel biomarker of DN.

scholarly journals The correlation of routine hematological indices with pterygium

2019 ◽  
Vol 11 ◽  
pp. 251584141984892 ◽  
Author(s):  
Bengi Ece Kurtul ◽  
Emrah Utku Kabatas ◽  
Serdar Ozates
Keyword(s):  
Oxidative Stress ◽  
Blood Count ◽  
Complete Blood Count ◽  
Density Lipoprotein ◽  
Control Group ◽  
Red Cell ◽  
Cell Distribution ◽  
Distribution Width ◽  
Hematological Indices ◽  
And Oxidative Stress

Purpose:Increased systemic/local inflammation and oxidative stress play a key role in the pathophysiology of pterygium, but there is limited information regarding routine hematological indices’ levels in patients with pterygium. In this study, we aimed to evaluate the levels of complete blood count parameters in patients with pterygium.Material and Method:In all, 61 patients with pterygium (pterygium group; mean age = 51.4 ± 13.8 years) and 55 healthy individuals (control group; mean age = 50.2 ± 13.1 years) were included in the study. Participants were given routine ophthalmic examinations; complete blood count parameters were assayed.Results:Compared to the control group, red cell distribution width level was significantly higher in patients with pterygium ( p = 0.009), but the difference between the groups in terms of the other complete blood count parameters was not statistically significant. However, high-density lipoprotein cholesterol level was significantly lower in the pterygium group than control group ( p = 0.015). In the pterygium group, low-density lipoprotein cholesterol levels were lower, but this difference was not statistically significant ( p = 0.079).Conclusion:Red cell distribution width levels were significantly increased in patients with pterygium. Our data support the idea that inflammation cytokines and oxidative stress may play an important role in the pathogenesis of this disorder.

scholarly journals TBHQ Alleviated Endoplasmic Reticulum Stress-Apoptosis and Oxidative Stress by PERK-Nrf2 Crosstalk in Methamphetamine-Induced Chronic Pulmonary Toxicity

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Yun Wang ◽  
Yu-Han Gu ◽  
Ming Liu ◽  
Yang Bai ◽  
Li-Ye Liang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Pulmonary Toxicity ◽  
Inflammatory Responses ◽  
Pulmonary Arteries ◽  
Treated Group ◽  
Control Group ◽  
Antioxidative Stress ◽  
And Oxidative Stress

Methamphetamine (MA) leads to cardiac and pulmonary toxicity expressed as increases in inflammatory responses and oxidative stress. However, some interactions may exist between oxidative stress and endoplasmic reticulum stress (ERS). The current study is designed to investigate if both oxidative stress and ERS are involved in MA-induced chronic pulmonary toxicity and if antioxidant tertiary butylhydroquinone (TBHQ) alleviated ERS-apoptosis and oxidative stress by PERK-Nrf2 crosstalk. In this study, the rats were randomly divided into control group, MA-treated group (MA), and MA plus TBHQ-treated group (MA + TBHQ). Chronic exposure to MA resulted in slower growth of weight and pulmonary toxicity of the rats by increasing the pulmonary arterial pressure, promoting the hypertrophy of right ventricle and the remodeling of pulmonary arteries. MA inhibited the Nrf2-mediated antioxidative stress by downregulation of Nrf2, GCS, and HO-1 and upregulation of SOD2. MA increased GRP78 to induce ERS. Overexpression and phosphorylation of PERK rapidly phosphorylated eIF2α, increased ATF4, CHOP, bax, caspase 3, and caspase 12, and decreased bcl-2. These changes can be reversed by antioxidant TBHQ through upregulating expression of Nrf2. The above results indicated that TBHQ can alleviate MA-induced oxidative stress which can accelerate ERS to initiate PERK-dependent apoptosis and that PERK/Nrf2 is likely to be the key crosstalk between oxidative stress and ERS in MA-induced chronic pulmonary toxicity.

Sign in / Sign up

Export Citation Format

Share Document