scholarly journals Amelioration of Paracetamol-Induced Hepatotoxicity in Rat by the Administration of Chloroform extract of Argemone mexicana

2019 ◽  
Vol 9 (4-s) ◽  
pp. 1232-1235
Author(s):  
Ganesh Virsen Taware ◽  
Kavita R Lokesh ◽  
Alok Pal Jain

Aim: The present study was undertaken to examine the effects of Chloroform extract of Argemone mexicana using the paracetamol-induced liver damage in rats as the animal model. Materials and methods: Chloroform extract of Argemone mexicana (100 and 200 mg/kg body weight) was administered daily in experimental animals. The hepatoprotective efficacy of Chloroform extract of Argemone mexicana (100 and 200 mg/kg) was investigated against paracetamol-induced hepatotoxicity. The levels of serum glutamic oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase (SGPT), serum alkaline phosphatase (ALP), bilirubin and triglycerides were estimated. Moreover, chloroform extract of Argemone mexicana -aided antioxidant defense against hepatotoxic insult of paracetamol was measured by evaluating a number of anti-oxidative biomarkers including reduced malondialdehyde (MDA) in the serum. Results: Oral administration of paracetamol (500 mg/kg b.wt.) resulted in a significant elevation of liver enzymes in serum such as SGOT, SGPT, ALP, bilirubin and triglyceride levels when compared with the results in the control group. As regards oxidative stress biomarkers, there were increased tissue levels of malondialdehyde in the group treated with paracetamol. All of these results were ameliorated by co-administration of chloroform extract of Argemone mexicana. Conclusions: These results suggest that the protective role of Chloroform extract of Argemone mexicana in the prevention of PCM-induced hepatic toxicity in rats was associated with a decrease of oxidative stress in hepatic tissues. Keywords: Antihepatotoxicity; Chloroform extract of Argemone mexicana; Paracetamol

2011 ◽  
Vol 31 (6) ◽  
pp. 565-573 ◽  
Author(s):  
M Tutanc ◽  
V Arica ◽  
N Yılmaz ◽  
A Nacar ◽  
I Zararsiz ◽  
...  

Aim: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Materials and methods: Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. Results: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. Conclusion: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Subhankari Prasad Chakraborty ◽  
Panchanan Pramanik ◽  
Somenath Roy

Staphylococcus aureus infection causes oxidative stress in neutrophils. The immune cells use reactive oxygen species (ROS) for carrying out their normal functions while an excess amount of ROS can attack cellular components that lead to cell damage. The present study was aimed to test the protective role of nanoconjugated vancomycin against vancomycin-sensitive Staphylococcus aureus (VSSA) and vancomycin-resistant Staphylococcus aureus (VRSA) infection induced oxidative stress in neutrophils. VSSA- and VRSA-infection were developed in Swiss mice by intraperitoneal injection of 5×106 CFU/mL bacterial solutions. Nanoconjugated vancomycin was treated to VSSA- and VRSA-infected mice at its effective dose for 10 days. Vancomycin was treated to VSSA and VRSA infected mice at similar dose, respectively, for 10 days. The result reveals that in vivo VSSA and VRSA infection significantly increases the level of lipid peroxidation, protein oxidation, oxidized glutathione level, and nitrite generation and decreases the level of reduced glutathione, antioxidant enzyme status, and glutathione-dependent enzymes as compared to control group; which were increased or decreased significantly near to normal in nanoconjugated vancomycin-treated group. These finding suggests the potential use and beneficial protective role of nanoconjugated vancomycin against VSSA and VRSA infection induced oxidative imbalance in neutrophils.


2014 ◽  
Vol 962-965 ◽  
pp. 1231-1234
Author(s):  
Hui Huang ◽  
Bo Qi

The objective of this study was to investigate the protective role of polysaccharide fromGynostemma pentaphyllumMakino (PGP) supplementation against exhaustive swimming exercise-induced oxidative stress. A total of 48 mice were randomly divided into four groups: control, low-dose, medium-dose, and high-dose PGP supplementation groups. The control group received distilled water and the supplementation groups received different doses of PGP (50, 100 and 200 mg/kg body weight) by gavage once a day for 28 consecutive days. After 28 days, the mice performed an exhaustive swimming exercise, and some biochemical parameters related to oxidative stress, including superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and malondialdehyde (MDA), were measured. The results showed that PGP supplementation could increase SOD, GPx and CAT contents, as well as decrease MDA contents in the liver and skeletal muscle of mice, which suggests that PGP supplementation has a protective role against exhaustive swimming exercise-induced oxidative stress.


2021 ◽  
Author(s):  
B. Brozek-Pluska ◽  
K. Beton

AbstractThe present study aimed to investigate the protective effect of β-carotene on the oxidative stress injury of human normal colon cell line CCD-18Co triggered by tert-Butyl hydroperoxide (tBHP). XTT examination was used to determine cell viability after β-carotene supplementation and to determine the optimal concentration of antioxidant in spectroscopic studies. Cell biochemistry for CCD-18Co control group, after tBHP adding and for cells in β-carotene - tBHP model was studied by using label-free Raman microspectroscopy. Results for stress treated CCD-18Co human colon normal cells and human colon cancer cells Caco-2 based on vibration features were also compared. Pretreatment with β-carotene alleviated damages in CCD-18Co human normal colon cells induced by tBHP and showed the preventative effect on cells apoptosis. Treatment with β-carotene altered the level of ROS investigated based on intensities of Raman peaks typical for lipids, proteins and nucleic acids. Presented study confirmed the antioxidant, protective role of β-carotene against ROS by using spectroscopic label-free Raman techniques.


2017 ◽  
Vol 104 (2) ◽  
pp. 139-149 ◽  
Author(s):  
M Savran ◽  
E Cicek ◽  
DK Doguc ◽  
H Asci ◽  
S Yesilot ◽  
...  

Like several other anticancer drugs, methotrexate (MTX) causes side effects, such as neuropathic pain, hepatotoxicity, and nephrotoxicity. Abnormal production of reactive oxygen species has been suspected in the pathophysiology of MTX-induced hepatorenal toxicity. Therefore, the aim of this study was to investigate the probable protective role of vitamin C (Vit C) on oxidative stress induced by MTX in the liver and kidney tissues of rats. A total of 32 rats were randomly and equally divided into four groups. The first group served as the control group. The second group received a single dose of 20 mg/kg of MTX intraperitoneally. To demonstrate our hypothesis, the third and the fourth groups received 250 mg/kg of Vit C for 3 days by oral gavage, with or without MTX treatment. At the end of the study, the liver and kidney tissues of the rats were collected and examined using histology. Both the tissues were assayed for malondialdehyde concentration and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities. In hepatic and renal tissues, lipid peroxidation levels were increased, whereas SOD, CAT, and GSH-Px levels were decreased by MTX. All parameters, including CAT levels in hepatic tissue, were significantly restored after the administration of Vit C for 3 days. Similar to the biochemical findings, evidence of oxidative damage was examined in both types of tissues by histopathological examination. From the results of this study, we were able to observe that Vit C administration modulates the antioxidant redox system and reduces the renal and hepatic oxidative stress induced by MTX. Vit C can ameliorate the toxic effect of MTX in liver and kidney tissues of rat.


2021 ◽  
Vol 11 (11) ◽  
pp. 4804
Author(s):  
Bassem M. Raafat ◽  
Walaa F. Alsanie ◽  
Abdulellah Al Thobaity ◽  
Abdulhakeem S. Alamri ◽  
Basem H. Elesawy ◽  
...  

Oxidative stress is a physiological imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify these products. Oxidative stress induced by ionizing radiation is one of the late biological effects of radiation. The aim of this study was to assess the protective role of Angelica archangelica and Ginkgo biloba extracts, which are commonly used as antioxidants in counteracting effects related to functional and non-functional hemoglobin derivative concentrations, as well as the rate of hemoglobin autoxidation before exposing rabbits to ionizing radiation. The experimental design included four groups of rabbits: a control group that did not receive gallium or antioxidants; Group 1, which received 68Ga isotope as a source of ionizing radiation with no prior treatment; Groups 2 and 3, which received A. archangelica and G. biloba root powder water extracts, respectively, for seven days prior to irradiation; and Group 4, which received a combined dose of both antioxidants, A. archangelica and G. biloba, prior to irradiation, with the same dose, time, and duration as used in Groups 2 and 3. The results demonstrate that both antioxidants had the ability to counteract oxidative stress induced by ionizing radiation, as well as to reduce the hemoglobin autoxidation rate. A synergistic effect was revealed when using a combined dose of both antioxidants at the same concentrations, times, and durations. A lower rate of free radical formation was also recorded, reflected by a reduction in superoxide dismutase (SOD) and glutathione peroxidase activity. The data here presented support the radioprotective role of both investigated antioxidants.


Author(s):  
Nesrine Djaber ◽  
Lynda Sabrina Ounaceur ◽  
Baya Nouha Moubine ◽  
Taha Khaldi ◽  
Mereim Rouag ◽  
...  

The present study was undertaken to evaluate the protective effects of Linum usitatissimum oil (LuO) against sub-chronic Roundup (RDP)-induced toxicity and oxidative stress in rats. Rats were divided into four groups: control group (no treatment), RDP group (Roundup at 269.9 mg/kg b.w.), LuO group (0.5 g/kg b.w. of LuO) and RDP+LuO group (RDP and LuO simultaneously). LuO decreased the ferric reducing antioxidant power (FRAP) (IC50=10.36 μg/ml) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) (IC50=22.85 mg/ml) in the tested tissues. The 30-day exposure of rats to RDP caused an increase in serum hepatic and renal markers: AST, ALT, ALP, LDH, γGT, bilirubin, urea, and creatinine. In addition, SOD, CAT and GST activities decreased by 43%, 61%, and 61%, respectively, while GPx activity, MDA and PCOs levels increased by 80%, 46%, 25%, respectively. LuO treatment alleviated hepatotoxicity in RDP-treated rats, showing improved levels of oxidative stress biomarkers and plasma biochemical parameters. The histological examination of the liver and kidney confirmed the changes in Roundup-treated rats and demonstrated the protective role of LuO.


2021 ◽  
Vol 80 (2) ◽  
pp. 164-172
Author(s):  
Cristina Iulia Mitran ◽  
Madalina Irina Mitran ◽  
Gabriela Loredana Popa

"Recent research has highlighted the role of oxidative stress in the pathogenesis of HPV-related lesions, especially in neoplastic diseases. Oxidative stress and chronic inflammation are the most important cofactors that HPV requires to persist and induce a malignant process. Data on the role of oxidative stress in benign lesions associated with HPV infection, such as genital and non-genital warts, is scarce and further research is needed. We have determined markers of oxidative stress in the serum of 26 patients with palmoplantar warts and 28 healthy subjects. We have investigated representative markers for the four main molecular targets of oxidative stress, nucleic acids – 8-hydroxy-2’-deoxyguanosine (8-OHdG), lipids – 4-hydroxynonenal (4-HNE), carbohydrates – pentosidine, and proteins – thiol-disulfide homeostasis parameters (TDHP): total thiol (TT), native thiol (NT), and disulfides (DS). The serum levels of oxidative stress markers, 4-HNE, 8-OHdG, and pentosidine, were statistically significantly higher in patients with warts in comparison to the control group (p < 0.01). Regarding TDHP, we have found that TT levels were statistically significantly higher in the patient group compared to the control one (p < 0.05). Even though NT and DS levels were reported to be higher in the patient group compared to the control one, no statistical significance was established (p > 0.05). Our results show enhanced oxidative stress damage in patients with palmoplantar warts and provide valuable data in understanding the molecular mechanisms involved in the pathogenesis of HPV infection. To the best of our knowledge, this is the first study to evaluate both 4-HNE and pentosidine in patients with palmoplantar warts. Keywords: oxidative stress, HPV, warts, thiol-disulfide homeostasis."


Folia Medica ◽  
2021 ◽  
Vol 63 (6) ◽  
pp. 928-931
Author(s):  
Kadir Soylemez ◽  
Fatih Temiz ◽  
Tahir Dalkiran ◽  
Yasar Kandur ◽  
Ergul Belge Kurutas ◽  
...  

Introduction: Henoch-Sch&ouml;nlein Purpura (HSP) is a systemic vasculitic syndrome characterized by non-thrombocytopenic purpura, arthritis/arthralgia, abdominal pain, and glomerulonephritis. The pathogenesis of HSP has not been clearly identified. Oxidative damage has a role in the pathogenesis of most cases. Aim: This study aimed to evaluate changes of oxidative stress by studying parameters like superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) in an attempt to identify the role of oxidative stress in HSP from another perspective. Materials and methods: This study enrolled 23 pediatric patients (ten girls and thirteen boys) diagnosed with HSP who were under follow-up at Sutcu Imam University School of Medicine Department of Pediatrics between 2014 and 2016 and twenty healthy children as the control group. The parents of all subjects gave informed consent to participate in the study. In the HSP group, the beginning season of the illness and the systemic involvement during follow-up were determined. Blood specimens were obtained at presentation before any treatment was started. SOD, CAT activities, and MDA values in erythrocyte and plasma samples were compared between the patient group and the healthy children. Results: Twenty-three patients with HSP (13 males, 10 females) and 20 healthy children participated in this study. The mean age of the HSP cases was 8.21&plusmn;3.78 years (range 2-16 years) and of the controls was 8.6&plusmn;4.2 (range 3-14 years). The mean MDA value was 2.95&plusmn;0.71 nmol/ml in the patient group and 2.67&plusmn;0.66 nmol/ml in the control group (p=0.787). The mean level of the CAT enzyme was 1.32&plusmn;0.35 U/g Hb in the patient group and 7.8&plusmn;1.74 U/g Hb in the control group (p=0.001). The mean levels of the SOD enzyme were 3.06&plusmn;0.85 U/g Hb in the patient group and 0.97&plusmn;0.36 U/g Hb in the control group (p=0.001). Conclusions: Although high MDA levels support the role of lipid peroxidation in the pathogenesis of HSP, statistical significance was not reached owing to a limited number of our patients. The reduced CAT enzyme activity is consistent with the findings of previous reports. This finding supports the notion that oxidative stress can play a role in the pathogenesis of HSP. Keypoints: Our findings support the notion that oxidative stress can play a role in the pathogenesis of HSP.


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