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

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.

Author(s):  
Medhat Mostafa Abozid ◽  
Hoda Ea Farid

 Objective: The current study was designed to estimate the potential protective role of the aqueous extract of rosemary (AER) (Rosmarinus officinalis) against trichloroacetic acid (TCA)-created hepatotoxicity in male albino rats.Methods: Forty male albino rats were separated into four groups of ten: Group I served as control; Group II was given AER (200 mg/kg/day) by gavage; Group III received TCA at the dose 50 mg/kg/day, and Group V was treated with AER (200 mg/kg/day) and received TCA (50 mg/kg/day). The experiment was carried out for 2 months.Results: The toxicity of TCA for rats was revealed by an elevation in liver marker enzymes activities (gamma-glutamyl transferase [GGT], alkaline phosphatase [ALP], aspartate transaminase [AST], alanine aminotransferase [ALT]) and conjugated bilirubin (CB) level, and a decrease in albumin and total protein (TP) levels. The TCA administration also caused a significant increase in the activities of catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD), and also malondialdehyde (MDA) level in liver tissues. These biochemical effects were accompanied by histological indicators of liver damage. Treatment with ARE recovered the liver damage instigated by TCA, as showed by perfection of liver enzyme markers (GGT, ALT, AST, ALP), CB, TP and albumin; as well as antioxidant parameters (CAT, SOD, GPx) and lipid peroxidation (MDA) and amelioration of histopathology changes in the liver tissues.Conclusion: It could be concluded that AER supplementation for 2 months in TCA-induced toxicity in rats benefited hepatic antioxidant status and improved liver injury and damage in male albino rats exposed to TCA.


Author(s):  
Tijani Stephanie Abiola ◽  
Olori Ogaraya David ◽  
Farombi Ebenezer Olatunde

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.


Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1031 ◽  
Author(s):  
Mohamed M. Abdel-Daim ◽  
Samah R. Khalil ◽  
Ashraf Awad ◽  
Ehsan H. Abu Zeid ◽  
Reda Abd El-Aziz ◽  
...  

This study aimed to describe the protective efficacy of Moringa oleifera ethanolic extract (MOEE) against the impact of cobalt chloride (CoCl2) exposure on the rat’s kidney. Fifty male rats were assigned to five equal groups: a control group, a MOEE-administered group (400 mg/kg body weight (bw), daily via gastric tube), a CoCl2-intoxicated group (300 mg/L, daily in drinking water), a protective group, and a therapeutic co-administered group that received MOEE prior to or following and concurrently with CoCl2, respectively. The antioxidant status indices (superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH)), oxidative stress markers (hydrogen peroxide (H2O2), 8-hydroxy-2-deoxyguanosine (8-OHdG), and malondialdehyde (MDA)), and inflammatory response markers (nitric oxide (NO), tumor necrosis factor (TNF-α), myeloperoxidase (MPO), and C-reactive protein (CRP)) were evaluated. The expression profiles of pro-inflammatory cytokines (nuclear factor-kappa B (NF-kB) and interleukin-6 (IL-6)) were also measured by real-time quantitative polymerase chain reaction (qRT-PCR). The results showed that CoCl2 exposure was associated with significant elevations of oxidative stress and inflammatory indices with reductions in the endogenous tissue antioxidants’ concentrations. Moreover, CoCl2 enhanced the activity of the NF-κB inflammatory-signaling pathway that plays a role in the associated inflammation of the kidney. MOEE ameliorated CoCl2-induced renal oxidative damage and inflammatory injury with the suppression of the mRNA expression pattern of pro-inflammatory cytokine-encoding genes. MOEE is more effective when it is administered with CoCl2 exposure as a prophylactic regimen. In conclusion, MOEE administration exhibited protective effects in counteracting CoCl2-induced renal injury in rats.


2016 ◽  
Vol 10 (1) ◽  
pp. 31-40
Author(s):  
Zeinab Sharifinasab ◽  
◽  
Mahdi Banaee ◽  
Mohammad Mohiseni ◽  
Ahmad Noori ◽  
...  

Background: Paraquat is nonselective bipyridyl herbicide that induces hepatotoxicity through oxidative stress. Vitamin C and chitosan have antioxidant as well as radical scavenger properties and show protective effects against reactive oxygen species (ROS). In the present study, hepatoprotective effects of chitosan and vitamin C were evaluated in common carp exposed to paraquat. Methods: While exposed to 0.02 mg. L-1paraquat for 21 days, common carp were fed chitosan (1000 mg. kg‑1 feed), vitamin C (1000 mg. kg-1 feed), and vitamin C combined with chitosan. At the end of the experiment, activities of hepatic enzymes and oxidative stress biomarkers were evaluated. Results: Paraquat induces changes in the activity of alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, alkaline phosphatase and lactate dehydrogenase in liver tissue of fish. However, these enzymes were restored to normal levels in fish fed with vitamin C and vitamin C combined with chitosan following exposure to paraquat. Increased levels of malondialdehyde were observed in liver after exposure to paraquat, while glucose-6-phosphate dehydrogenase and catalase activities and the total antioxidant levels decreased. Administration of vitamin C combined with chitosan significantly reduced malondialdehyde levels and increased the total antioxidant capacity, glucose-6-phosphate dehydrogenase and catalase activities. Conclusion: Administration of vitamin C is effective in reducing liver toxicity of paraquat. However, administrating both vitamin C and chitosan is more effective. In other words, chitosan and vitamin C have a synergic effect. They could be used as hepatoprotective agents against paraquat-induced hepatotoxicity in fish.


2021 ◽  
Vol 10 (1) ◽  
pp. 31-36

The present study was carried out to investigate and compare the effect of nicotine alone and in combination with melatonin on some oxidants and antioxidant parameters, histopathological changes and DNA integrity in the liver and kidneys of male rats. For this purpose 75 mature male rats weighing 120-140g were randomly divided into five groups; control group (1% ethanol in saline), nicotine group (rats administrated nicotine at a dose of 0.6mg/kg body weight; BW) and nicotine and melatonin groups (rats administrated the same dose of nicotine plus 1, 5 or 10mg/kg BW melatonin, respectively). Nicotine and ‏ melatonin were injected intraperitoneally daily for 21days. Fasting blood samples were collected from each rat one day after the end of last injection (at 22nd day) and sera were collected for determination of total antioxidant capacity (TAC). Five rats were sacrificed from each group; Liver and kidneys were collected for estimation of oxidative stress parameters (MDA, SOD and GSH), histopathological examination and for estimation of DNA damage. The results revealed that nicotine increased MDA, decreased TAC, SOD and GSH, induced histopathological changes and increased the percentage of DNA damage in the liver and kidneys Melatonin administration with nicotine counteracted the effect of nicotine on previous parameters. The effect of melatonin was dose dependent and the 10mg dose produced the highest protective effect. It is concluded that melatonin can ameliorate the harmful effect of nicotine on the liver and kidneys of male rats.


2018 ◽  
Vol 16 (1) ◽  
pp. 133-140 ◽  
Author(s):  
Riaz Ullah ◽  
Mansour S. Alsaid ◽  
Abdelaaty A. Shahat ◽  
Almoqbil Abdulaziz Naser ◽  
Abdullah A. Al-Mishari ◽  
...  

AbstractThe detoxification, metabolism, and excretion of various endogenous and exogenous materials occur mainly in the liver. Liver diseases are a global concern, and classified as chronic hepatitis, cirrhosis, and hepatosis. The development of safe hepatoprotective agents remains an unmet need. Therefore, we investigated the antioxidant effects of methanolic and n-hexane fractions of Zilla spinosa (ZSM and ZSH, respectively) and Hammada elegans (HEM and HEH, respectively) against carbon tetrachloride (CCl4)-induced liver toxicity in rats. Antioxidant activity was studied by the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay. The rats were divided into 11 groups (n=6)–group, 1 (control), group 2 (CCl4 only), group 3 (CCl4+silymarin 10 mg/kg), group 4 (CCl4+HEM 250 mg/kg), group 5 (CC14+HEM 500 mg/kg), group 6 (CCl4+HEH 250 mg/kg), group, 7 (CCl4+HEH 500 mg/kg), group, 8 (CCl4+ZSM 250 mg/kg), group 9 (CCl4+ZSM 500 mg/kg), group 10 (CCl4+ZSH 250 mg/kg), and group 11 (CCl4+ZSH 500 mg/kg). Serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma glutamyl transferase, and total bilirubin were measured. The extent of hepatic injury was histopathologically assessed. Treatment with ZSM and ZSH at 250 and 500 mg/kg did not significantly affect biochemical results compared with the CCl4 only group. However, treatment with both HEM and HEH at 250 and 500 mg/kg provided significant (p<0.001) results compared with the CCl4 only group. These results were consistent with histological findings. HEM and HEH at 250 μg/mL significantly inhibited DPPH radical formation by 38.E6 and 35.65%, rerpectively. However antioxidant effects of ZSM and ZSH were insignificant.


Coatings ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 594
Author(s):  
Najah M. Al-Baqami ◽  
Reham Z. Hamza

Cadmium (Cd) is widely used in some industries and emitted from fossil fuels. It is a heavy metal with a number of side effects, including hepatotoxicity. Resveratrol (Rs) is considered an important polyphenol, which is a secondary plant metabolite and has the ability to scavenge free radicals. The study was designed to evaluate the effects of resveratrol on Cd, which induced hepatotoxicity, by the assessment of some histopathological and biochemical alterations. Forty male albino rats were divided into four groups: the 1st group was the control group, the 2nd group was treated with Cd (5 mg/kg), the 3rd group was given Rs (20 mg/kg), and the 4th group was treated with Cd in combination with Rs intraperitoneally for 30 successive days. The results indicate that Cd increased liver enzymes alanine aminotransferase and aspartate aminotransferase (AST and ALT), alkaline phosphatase ALP and gamma-glutamyl transferase (γ-GT) while reducing the total protein level; Cd increased the malondialdhyde (MDA) level while decreasing the levels of other antioxidant enzymes super oxide dismutase, catalase and glutathione peroxidase (SOD, CAT and GPx). Serious congestion and hemorrhage related to the hepatic tissues were noticed in the Cd group, and Rs plays a major role in alleviating histopathological injuries and hepatic oxidative damage. It is clear that Rs has the ability to minimize the hepatotoxicity induced by Cd in male rats.


2021 ◽  
Vol 5 (1) ◽  
pp. 27
Author(s):  
Tijani Stephanie Abiola ◽  
Olori Ogaraya David ◽  
Farombi Ebenezer Olatunde

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


2021 ◽  
Vol 46 (2) ◽  
Author(s):  
O. A Dosumu ◽  
D. I. Akinloye ◽  
O. B. Onunkwor ◽  
F. C. Thomas ◽  
R. A. Adeyemo

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.


2019 ◽  
Vol 8 (3) ◽  
pp. 231-237 ◽  
Author(s):  
Pantea Ramezannezhad ◽  
Ali Nouri ◽  
Esfandiar Heidarian

Introduction: Diclofenac (DIC) is one of the compounds derived from acetic acid which isknown for its anti-inflammatory and analgesic attributes. Silymarin is a flavonoid compoundwhich is derivate from Silybum marianum seeds. This research was done to assess the protectiverole of silymarin against liver toxicity induced by DIC in male rats.Methods: Randomly, 40 male Wistar rats were assigned into five groups as follows: Group 1:control group, Group 2: DIC-only treated (50 mg/kg, i.p), Group 3: silymarin-only treated (200mg/kg, p.o); Groups 4 and 5: DIC (50 mg/kg, i.p) plus silymarin (100 mg/kg and 200 mg/kg, p.o,respectively) treated. Various biochemical, molecular, and histological parameters were evaluatedin serum and tissue.Results: In the DIC-only treated group, the levels of liver glutathione peroxidase (GPx), superoxidedismutase (SOD), intracellular glutathione (GSH) and catalase (CAT) significantly diminished andthe levels of total bilirubin, alkaline phosphatase (ALP), nitrite, alanine aminotransferase (ALT),malondialdehyde (MDA), serum tumor necrosis factor-α (TNF-α), aspartate aminotransferase(AST), and TNF-α gene expression were remarkably elevated relative to control animals. In otherhands, treatment with silymarin caused a noticeable elevation in GPx, SOD, GSH, CAT and aremarkable reduction in levels of total bilirubin, ALP, nitrite content, ALT, MDA, serum TNF-α,AST and TNF-α gene expression relative to DIC-only treated group. Histopathological injurieswere also improved by silymarin administration.Conclusion: The results confirm that silymarin has an ameliorative effect on liver toxicity inducedby DIC and oxidative stress in male rats.


Sign in / Sign up

Export Citation Format

Share Document