scholarly journals Protective Effects of Chlorogenic Acid against Carbon Tetrachloride-Induced Hepatotoxicity in Mice

Processes ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 31
Author(s):  
Yu-Wen Hsu ◽  
Ya-Yu Chen ◽  
Chia-Fang Tsai
Keyword(s):  
Lipid Peroxidation ◽  
Carbon Tetrachloride ◽  
Chlorogenic Acid ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Protective Effects ◽  
Thiobarbituric Acid Reactive Substances ◽  
Liver Injuries ◽  
Severe Impairment ◽  
Ccl4 Administration

The protective effects of chlorogenic acid (CGA) against liver injury were evaluated by its reduction in carbon tetrachloride (CCl4)-induced hepatic damage in ICR mice. The animals were orally given CGA (60, 100, and 200 mg/kg, respectively) or silymairn (200 mg/kg) daily with 0.3% CCl4 administration (3 mL/kg, dissolved in olive oil) after medicament treatment on the 7th day. Compared with the normal group, CCl4 caused severe impairment in liver according to the evidence of significant reduction in the level of total albumin and expansion (p < 0.05) of the activities in aspartate aminotransferase (AST) and alanine aminotransferase (ALT), cholesterol, triglyceride (TG), and total albumin in serum, decreased the level of glutathione (GSH), and diminished the activities of catalase, superoxide dismutase (SOD), glutathione reductase (GSH-Rd), and glutathione peroxidase (GSH-Px) in liver while increasing the level of hepatic thiobarbituric acid-reactive substances (TBARS). However, oral administration of CGA or silymarin could significantly (p < 0.05) decrease the serum levels of AST, ALT, cholesterol, TG, and total albumin and elevated the serum total albumin and the activities of GSH, catalase, SOD, GSH-Rd, and GSH-Px while leading to decline the TBARS in liver compared with CCl4-intoxicated group. Moreover, histopathology displayed that CGA decreased the formation of lesions in liver resulted from CCl4. The outcomes indicate that CGA shows the efficiency hepatoprotective consequences for CCl4-incited liver injuries in mice by the elevation of the activities of antioxidant enzymes and hindrance of lipid peroxidation.

Endothelium-dependent vasodilation in the brachial artery is impaired in smokers: effect of vitamin C

1997 ◽  
Vol 273 (4) ◽  
pp. H1644-H1650 ◽  
Author(s):  
Takeshi Motoyama ◽  
Hiroaki Kawano ◽  
Kiyotaka Kugiyama ◽  
Osamu Hirashima ◽  
Masamichi Ohgushi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cigarette Smoking ◽  
Vitamin C ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Sublingual Nitroglycerin ◽  
Thiobarbituric Acid Reactive Substances ◽  
Lower Vitamin

Cigarette smoking has been shown to cause endothelial dysfunction. To examine the effects of vitamin C and cigarette smoking on endothelium-dependent vasodilation, we measured the lumen diameter and flow velocity of the brachial arteries at rest, during reactive hyperemia following transient arterial occlusion, and after sublingual nitroglycerin (0.3 mg) in smokers ( n = 20) and nonsmokers ( n = 20) with high-resolution ultrasound after infusion of saline or saline plus vitamin C (10 mg/min for 20 min). We also performed the same study in smokers ( n = 15) before and 10 min after cigarette smoking. In addition, we measured the serum levels of vitamin C and the plasma levels of thiobarbituric acid-reactive substances (TBARS) as an index of lipid peroxidation. The smokers had lower vitamin C levels, higher TBARS levels, and showed impairment of flow-dependent vasodilation (5.3 ± 1.9 vs. 9.2 ± 1.5%, P < 0.0001) compared with nonsmokers. Vitamin C administration improved the impairment of flow-dependent vasodilation (5.3 ± 1.9 to 9.0 ± 3.2%, P < 0.001) and decreased TBARS in smokers but not in nonsmokers. Furthermore, cigarette smoking acutely worsened the impairment of flow-dependent vasodilation (5.4 ± 1.8 to 1.5 ± 1.3%, P < 0.01) and increased TBARS. We conclude that 1) endothelium-dependent vasodilation in the brachial arteries is impaired in smokers and this impairment is improved by vitamin C administration in association with a decrease in TBARS and 2) cigarette smoking produces acute impairment of endothelium-dependent vasodilation in smokers in association with an increase in TBARS.

Free Phenolic Acids from the Seaweed Halimeda monile with Antioxidant Effect Protecting against Liver Injury

2009 ◽  
Vol 64 (9-10) ◽  
pp. 657-663 ◽  
Author(s):  
Jorge Mancini-Filho ◽  
Alexis Vidal Novoa ◽  
Ana Elsa Batista González ◽  
Elma Regina S de Andrade-Wartha ◽  
Dalva Assunção Portari Mancini
Keyword(s):  
Antioxidant Activity ◽  
Phenolic Acids ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substances ◽  
Chemical Agents ◽  
Liver Injuries ◽  
Dpph Method ◽  
Other Substances ◽  
Free Phenolic Acids

Phenolic compounds are found in seaweed species together with other substances presenting antioxidant activity. The objective of this work was to evaluate the antioxidant activity of the free phenolic acids (FPA) fraction from the seaweed Halimeda monile, and its activity to protect the expression of hepatic enzymes in rats, under experimental CCl4 injury. The antioxidant activity was measured by the DPPH method. The FPA fraction (80 mg/kg, p.o.) was administered during 20 consecutive days to rats. The peroxidation was performed by thiobarbituric acid reactive substances (TBARS). The SOD and CAT enzymatic expressions were measured by RT/PCR. The histology technique was used to evaluate liver injuries. The expression of both, CAT and SOD genes, was more preserved by FPA. Only partial injury could be observed by histology in the liver of rats receiving FPA as compared with the control group; and CCl4 administration induced 60% more peroxidation as compared with the rats receiving FPA. These data suggest that FPA could modulate the antioxidant enzymes and oxidative status in the liver through protection against adverse effects induced by chemical agents

scholarly journals Biochemical Studies on Phenylhydrazine Induced Experimental Anemic Albino Rats

2015 ◽  
Vol 3 (1) ◽  
pp. 41-47
Author(s):  
Nirjala Laxmi Madhikarmi ◽  
Kora Rudraiah Siddalinga Murthy
Keyword(s):  
Lipid Peroxidation ◽  
Lipid Hydroperoxide ◽  
Thiobarbituric Acid ◽  
Albino Rats ◽  
Enzymatic Antioxidants ◽  
Medical Sciences ◽  
Thiobarbituric Acid Reactive Substances ◽  
Biochemical Studies ◽  
Healthy Control ◽  
Wistar Albino Rats

INTRODUCTION: The present study evaluated the modulatory effects of diphenylhydrazine induced experimental wistar albino rats and also to assess various biochemical parameters in whole blood and red blood cell lysate.MATERIALAND METHODS: Twenty male albino rats weighing 180-200 gm were selected for the study and divided in two groups; ten phenylhydrazine dihydrochloride (PHZ) induced anemia and ten healthy control. Thiobarbituric acid reactive substances and lipid hydroperoxide were measured as lipid peroxidation parameter. The antioxidant vitamins A, C and E and enzymatic antioxidants; catalase, glutathione peroxidase and superoxide dismutase were also assessed.RESULTS: Phenylhydrazine induced anemic rats showed a significant increase in the lipid peroxidation and decrease in the antioxidants as compared to healthy rats.CONCLUSION: The study concludes that phenylhydrazine induced experimental anemic albino rats showed increased oxidative stress than compared with healthy albino rats.Journal of Universal College of Medical Sciences Vol. 3, No. 1, 2015: 41-47 

Bitter Melon Protects Against Lipid Peroxidation Caused by Immobilization Stress in Albino Rats

2009 ◽  
Vol 79 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Chaturvedi
Keyword(s):  
Lipid Peroxidation ◽  
Immobilization Stress ◽  
Reduced Glutathione ◽  
Cumene Hydroperoxide ◽  
Liver Homogenate ◽  
Thiobarbituric Acid ◽  
Albino Rats ◽  
Bitter Melon ◽  
Protective Effects

In the present study, protective effects of bitter melon (Momordica charantia) extract on lipid peroxidation induced by immobilization stress in rats have been assessed. Graded doses of extract (50, 100, and 150 mg/kg body weight) were administered orally to rats subjected to immobilization stress for two hours for seven consecutive days. Stress was applied by keeping the rats in a cage where no movement was possible. After seven days, rats were killed by decapitation after ether anesthesia. Blood and liver were collected to measure thiobarbituric acid reactive substances, reduced glutathione, and catalase. In vitro effects of M. charantia extract on lipid peroxidation in liver homogenate of normal, control, and rats pretreated with extract were carried out against cumene hydroperoxide-induced lipid peroxidation. Results reveal that in vivo M. charantia inhibited stress-induced lipid peroxidation by increasing the levels of reduced glutathione and activities of catalase. These results were further supported by in vitro results. In vitro inhibition of lipid peroxidation was indicated by low levels of thiobarbituric acid in the liver homogenate from pretreated rats and normal rats when incubated with both cumene hydroperoxide and extract. Inhibition was also noted in the homogenate where the rats were pretreated but the mixture contained no extract. Thus this plant provides protection by strengthening the antioxidants like reduced glutathione and catalase. Inclusion of this plant in the daily diet would be beneficial.

scholarly journals Plasma Lipid Peroxidation as a Marker for Seminal Oxidative Stress in Stallion

2019 ◽  
Vol 11 (6) ◽  
pp. 401
Author(s):  
Patricia Wolkmer ◽  
Andressa M. G. Stumm ◽  
Luiz F. K. Borges ◽  
Eduarda P. T. Ferreira ◽  
Bruna Favaretto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Seminal Plasma ◽  
Plasma Lipid ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Semen Collection ◽  
Semen Storage ◽  
Plasma Lipid Peroxidation ◽  
Antioxidant Enzyme Catalase

This experiment aims to evaluate the correlation between lipid peroxidation levels in serum and seminal plasma in equines. Also, it investigates the lipid peroxidation in extended semen samples and its effects and sperm motility during a 72 hr refrigeration period. Blood and semen were collected from fertile Crioulo stallions. Serum and seminal plasma lipid peroxidation levels were analyzed by thiobarbituric acid reactive substances (TBARS) immediately after semen collection. After addition of extender (hour = 0), diluted semen was refrigerated and stored at 5 &deg;C. Semen analyses, TBARS and catalase activity were performed in extended semen at 0, 24, 48, and 72 hours. We noted that levels of plasma lipid peroxidation can be used as an indicative of seminal oxidative stress. Also, lipid peroxidation does not increase substantially during semen storage. Lipid peroxidation and the antioxidant enzyme catalase do not seem to be the major cause of loss and motility and consequently reduction in fertility in stallion semen during storage for 72 h at 5 &deg;C.

Oxypurinol administration fails to prevent free radical-mediated lipid peroxidation during loaded breathing

1999 ◽  
Vol 87 (3) ◽  
pp. 1123-1131 ◽  
Author(s):  
G. Supinski ◽  
D. Nethery ◽  
D. Stofan ◽  
L. Szweda ◽  
A. DiMarco
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Xanthine Oxidase ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Xanthine Oxidase Inhibitor ◽  
Air Breathing ◽  
Fatigue Development ◽  
Loaded Breathing

The purpose of the present study was to determine whether it is possible to alter the development of fatigue and ablate free radical-mediated lipid peroxidation of the diaphragm during loaded breathing by administering oxypurinol, a xanthine oxidase inhibitor. We studied 1) room-air-breathing decerebrate, unanesthetized rats given either saline or oxypurinol (50 mg/kg) and loaded with a large inspiratory resistance until airway pressure had fallen by 50% and 2) unloaded saline- and oxypurinol-treated room-air-breathing control animals. Additional sets of studies were performed with animals breathing 100% oxygen. Animals were killed at the conclusion of loading, and diaphragmatic samples were obtained for determination of thiobarbituric acid-reactive substances and assessment of in vitro force generation. We found that loading of saline-treated animals resulted in significant diaphragmatic fatigue and thiobarbituric acid-reactive substances formation ( P < 0.01). Oxypurinol administration, however, failed to increase load trial time, reduce fatigue development, or prevent lipid peroxidation in either room-air-breathing or oxygen-breathing animals. These data suggest that xanthine oxidase-dependent pathways do not generate physiologically significant levels of free radicals during the type of inspiratory resistive loading examined in this study.

scholarly journals Gene expression in human small intestinal mucosa in vivo is mediated by iron-induced oxidative stress

2006 ◽  
Vol 25 (2) ◽  
pp. 242-249 ◽  
Author(s):  
Freddy J. Troost ◽  
Robert-Jan M. Brummer ◽  
Guido R. M. M. Haenen ◽  
Aalt Bast ◽  
Rachel I. van Haaften ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Lipid Peroxidation ◽  
Small Intestine ◽  
Antioxidant Capacity ◽  
Intestinal Mucosa ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Oxidative Challenge ◽  
Gene Reporters

Iron-induced oxidative stress in the small intestine may alter gene expression in the intestinal mucosa. The present study aimed to determine which genes are mediated by an iron-induced oxidative challenge in the human small intestine. Eight healthy volunteers [22 yr(SD2)] were tested on two separate occasions in a randomized crossover design. After duodenal tissue sampling by gastroduodenoscopy, a perfusion catheter was inserted orogastrically to perfuse a 40-cm segment of the proximal small intestine with saline and, subsequently, with either 80 or 400 mg of iron as ferrous gluconate. After the intestinal perfusion, a second duodenal tissue sample was obtained. Thiobarbituric acid-reactive substances, an indicator of lipid peroxidation, in intestinal fluid samples increased significantly and dose dependently at 30 min after the start of perfusion with 80 or 400 mg of iron, respectively ( P < 0.001). During the perfusion with 400 mg of iron, the increase in thiobarbituric acid-reactive substances was accompanied by a significant, momentary rise in trolox equivalent antioxidant capacity, an indicator of total antioxidant capacity ( P < 0.05). The expression of 89 gene reporters was significantly altered by both iron interventions. Functional mapping showed that both iron dosages mediated six distinct processes. Three of those processes involved G-protein receptor coupled pathways. The other processes were associated with cell cycle, complement activation, and calcium channels. Iron administration in the small intestine induced dose-dependent lipid peroxidation and a momentary antioxidant response in the lumen, mediated the expression of at least 89 individual gene reporters, and affected at least six biological processes.

scholarly journals Protective effects of honey and bee venom against lipopolysaccharide and carbon tetrachloride-induced hepatoxicity and lipid peroxidation in rats

2020 ◽  
Vol 9 (5) ◽  
pp. 693-705
Author(s):  
Noha M Meligi ◽  
Suzan Alaa Ismail ◽  
Nagy S Tawfik
Keyword(s):  
Lipid Peroxidation ◽  
Carbon Tetrachloride ◽  
Hematological Parameters ◽  
Lipid Peroxide ◽  
Alpha Fetoprotein ◽  
Bee Venom ◽  
Albino Rats ◽  
Average Weight ◽  
Protective Effects ◽  
Liver Histopathology

Abstract In the present study, the protective effects of honey and bee venom (BV) either independently or in combination against lipopolysaccharide (LPS) and carbon tetrachloride (CCl4)-induced hepatoxicity, lipid peroxidation, and hematological alterations in male albino rats were investigated. In addition, histopathological alterations of hepatic tissues induced by LPS/CCL4 were recorded. Sixty-four of male albino rats of average weight 120–150 g were included in this study. Rats were divided into eight equal groups of eight. The obtained results demonstrated that treatment with LPS/CCl4 caused an increase in the levels of alpha-fetoprotein, which was accompanied by changes in the hepatic function biomarkers that characterized by the increased levels of transaminases (AST, ALT). The results showed oxidative stress as assigned by the increase in lipid peroxide. Meantime detraction in the antioxidants, including glutathione peroxidase was observed. Interruptions in biochemical parameters accompanied by disturbances in hematological parameters and liver histopathology were resulted due to exposure to LPS/CCl4. This study showed the use of honey and BV provided a protective effect on hepatotoxicity induced by LPS/CCl4. This might have been occurred through the reduction of hepatic transaminases and the “Alpha-fetoprotein” in serum and the equilibration of the antioxidation system, thereby, inhibiting the reactive oxygen species accumulation. Honey and BV administration reestablish disturbed hematological parameters and liver histopathology persuaded by LPS/CCl4. More interesting, we demonstrated that using a combination of the honey and BV showed promising enhancement in their protective effects over the use of just one of the two reagents.

Lipid Peroxidation and Cherniluminescence during Naproxen Metabolism in Rat Liver Microsomes

1994 ◽  
Vol 13 (12) ◽  
pp. 831-838 ◽  
Author(s):  
Hiroyuki Yokoyama ◽  
Toshiharu Horie ◽  
Shoji Awazu
Keyword(s):  
Lipid Peroxidation ◽  
Singlet Oxygen ◽  
Rat Liver ◽  
Liver Microsomes ◽  
Thiobarbituric Acid ◽  
Rat Liver Microsomes ◽  
Oxygen Species ◽  
Thiobarbituric Acid Reactive Substances ◽  
Microsomal Suspension ◽  
Weight Protein

1 Rat liver microsomal suspension containing NADPH and MgCl2 was incubated at 37°C with naproxen, a non-steroidal anti-inflammatory drug. Thiobarbituric acid reactive substances (TBA-RS), high molecular weight protein aggregates and fluorescent substances were formed in the microsomal suspension. 2 Chemiluminescence was produced from the microsomal suspension. This chemiluminescence production was well correlated to the TBA-RS formation, indicating that the chemiluminescence production was closely associated with the lipid peroxidation. 3 The addition of SKF-525A to the microsomal suspension inhibited the production of TBA-RS, chemiluminescence and 6-demethylnaproxen (6-DMN), the oxidative product of naproxen. Further, the antioxidant, α-tocopherol and singlet oxygen quenchers like histidine, dimethylfuran and 1,4-diazabicyclo[2,2,2]octane strikingly inhibited the productions of chemiluminescence and TBA-RS. 4 Neither naproxen nor 6-DMN caused lipid peroxidation in the absence of NADPH. Thus, lipid peroxidation and chemiluminescence during the oxidation of naproxen in liver microsomes was suggested to be provoked by reactive oxygen species and an origin of chemiluminescence was shown to be singlet oxygen.

Sign in / Sign up

Export Citation Format

Share Document