scholarly journals Mate Tea Prevents Oxidative Stress in the Blood and Hippocampus of Rats with Acute or Chronic Ethanol Administration

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Bianca Scolaro ◽  
Daniela Delwing-de Lima ◽  
José Geraldo Pereira da Cruz ◽  
Débora Delwing-Dal Magro
Keyword(s):  
Oxidative Stress ◽  
Chronic Administration ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Chronic Ethanol Administration ◽  
Mate Tea

Objective. The aim of this study was to evaluate the influence of acute and chronic intake of mate tea on the effects elicited by acute and chronic administration of ethanol.Methods. Oxidative stress was evaluated by measuring thiobarbituric acid-reactive substances (TBARS), as well as the activities of the antioxidant enzymes, catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in the hippocampus and blood of rats. Male Wistar rats were randomly assigned to four groups, for both acute and chronic treatment: (1) control group, (2) treated group, (3) intoxicated group, (4) and intoxicated group treated with mate tea.Results. Both ethanol administrations significantly increased TBARS in plasma and hippocampus of rats and altered antioxidant enzyme activities, changes which were reverted by mate tea administration.Conclusions. Data indicate that acute and chronic ethanol administration induced oxidative stress in hippocampus and blood and that mate tea treatment was able to prevent this situation.

scholarly journals Alteration of oxidative-stress and related marker levels in mouse colonic tissues and fecal microbiota structures with chronic ethanol administration: Implications for the pathogenesis of ethanol-related colorectal cancer

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0246580
Author(s):  
Hideo Ohira ◽  
Atsuki Tsuruya ◽  
Daiki Oikawa ◽  
Wao Nakagawa ◽  
Rie Mamoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Chronic Administration ◽  
Ethanol Consumption ◽  
Treg Cells ◽  
Fecal Microbiota ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Chronic Ethanol Consumption ◽  
Chronic Ethanol Administration

Chronic ethanol consumption is a risk factor for colorectal cancer, and ethanol-induced reactive oxygen species have been suggested to play important roles in the pathogenesis of ethanol-related colorectal cancer (ER-CRC). In this study, the effects of 10-week chronic administration of ethanol on the colonic levels of oxidative stress and advance glycation end product (AGE) levels, as well as fecal microbiota structures, were examined in a mouse model. Chronic oral administration of ethanol in mice (1.0 mL of 1.5% or 5.0% ethanol (v/v) per day per mouse, up to 10 weeks) resulted in the elevation of colonic levels of oxidative stress markers (such as 8-hydroxy-2’-deoxyguanosine and 4-hydroxynonenal) compared to control mice, and this was consistently accompanied by elevated levels of inflammation-associated cytokines and immune cells (Th17 and macrophages) and a decreased level of regulatory T (Treg) cells to produce colonic lesions. It also resulted in an alteration of mouse fecal microbiota structures, reminiscent of the alterations observed in human inflammatory bowel disease, and this appeared to be consistent with the proposed sustained generation of oxidative stress in the colonic environment during chronic ethanol consumption. Moreover, the first experimental evidence that chronic ethanol administration results in elevated levels of advanced glycation end products (AGEs) and their receptors (RAGE) in the colonic tissues in mice is also shown, implying enhanced RAGE-mediated signaling with chronic ethanol administration. The RAGE-mediated signaling pathway has thus far been implicated as a link between the accumulation of AGEs and the development of many types of chronic colitis and cancers. Thus, enhancement of this pathway likely exacerbates the ethanol-induced inflammatory states of colonic tissues and might at least partly contribute to the pathogenesis of ER-CRC.

Effects of chronic ethanol administration on rat liver proteasome activities: Relationship with oxidative stress

Hepatology ◽  
1999 ◽  
Vol 29 (1) ◽  
pp. 14-20 ◽  
Author(s):  
Virginie Fataccioli ◽  
Evelyne Andraud ◽  
Monique Gentil ◽  
Samuel W. French ◽  
Helene Rouach
Keyword(s):  
Oxidative Stress ◽  
Rat Liver ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Chronic Ethanol Administration

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.

Acute and chronic ethanol on hepatic oxygen ethanol and lactate metabolism in cats

1990 ◽  
Vol 258 (3) ◽  
pp. G411-G418 ◽  
Author(s):  
C. V. Greenway ◽  
W. W. Lautt
Keyword(s):  
Venous Blood ◽  
Chronic Administration ◽  
Chronic Ethanol ◽  
Ethanol Metabolism ◽  
Ethanol Administration ◽  
Control Group ◽  
Base Line ◽  
Acute Administration ◽  
Lactate Metabolism ◽  
O2 Uptake

The effects of increasing blood ethanol levels on hepatic hemodynamics and O2, ethanol, and lactate metabolism were studied in two groups of anesthetized cats: a control group and a group whose prior fluid intake contained 2, 4, then 8% ethanol for 24 days. Within each group, responses were compared in cats with acutely denervated and innervated livers. A hepatic venous long-circuit technique with an extracorporeal reservoir was used to allow hemodynamic measurements and repeated sampling of arterial, portal, and hepatic venous blood without depletion of the cats' blood volume. Vmax for ethanol was 105 +/- 9 and 91 +/- 6 mumol.min-1 g liver-1 and Km was 136 +/- 18 and 168 +/- 24 microM for control and chronic alcohol groups, respectively. There was no stimulation of ethanol metabolism after chronic administration. O2 uptake by the liver was not altered during acute ethanol administration in any group and base-line O2 uptakes before acute administration of ethanol were not different between normal and chronic ethanol groups. No evidence for a hypermetabolic state induced by chronic ethanol administration was seen in innervated or acutely denervated livers. Oxidation of ethanol required 40-45% of normal O2 uptake; thus other oxidative processes must have been suppressed during ethanol metabolism. Hepatic lactate uptake remained unaltered when ethanol metabolism was less than 0.5 Vmax, but was suppressed on an equimolar basis with ethanol metabolism when ethanol metabolism rose to greater than 0.5 Vmax. Thus lactate metabolism is one process that can be suppressed to allow ethanol metabolism without additional O2 uptake by the liver.

The effects of hydraulic calcium silicate containing endodontic materials on oxidative stress in erythrocytes and liver

2017 ◽  
Vol 43 (3) ◽  
pp. 333-341 ◽  
Author(s):  
Kadriye Demirkaya ◽  
Birsen Can Demirdöğen ◽  
Zeynep Öncel Torun ◽  
Onur Erdem ◽  
Yaşar Meriç Tunca
Keyword(s):  
Oxidative Stress ◽  
Calcium Silicate ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Thiobarbituric Acid Reactive Substances ◽  
Dental Cement ◽  
Oxidative Stress Parameters ◽  
Liver Tbars ◽  
Stress Parameters

Abstract Objective: The aim of this study was to evaluate the effects of hydraulic calcium silicate endodontic cements, MTA Angelus, MTA Fillapex, and Theracal LC, on erythrocyte and liver oxidative stress parameters of rats. Methods: Right upper incisor of each rat was extracted and polyethylene tubes containing the dental cements, or left empty for the control group, were inserted into the extraction socket. Blood and liver samples of each animal were obtained after 7, 30, or 60 days. Thiobarbituric acid reactive substances (TBARS) levels and catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities were determined by spectrophotometry. Results: Erythrocyte and liver TBARS levels, and CAT and SOD enzymatic activities were significantly increased in dental cement applied groups compared with controls on day 7. The highest erythrocyte and liver TBARS concentrations were observed in the MTA Angelus group on day 7 of exposure. On day 30, erythrocyte CAT activity remained markedly high, but the other parameters returned to almost normal levels. On day 60, all parameters were similar between the control and the experimental groups. Conclusions: This is the first study to show that TBARS levels and antioxidant enzyme activities are transiently increased as a result of dental cement application.

scholarly journals Melatonin protects the liver and erythrocytes against oxidative stress in cirrhotic rats

2010 ◽  
Vol 47 (1) ◽  
pp. 72-78 ◽  
Author(s):  
Darlan Pase da Rosa ◽  
Silvia Bona ◽  
Douglas Simonetto ◽  
Claudio Zettler ◽  
Cláudio Augusto Marroni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Carbon Tetrachloride ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Hepatic Tissue ◽  
Control Group ◽  
Significant Impairment ◽  
Peroxidase Enzymes ◽  
Cirrhotic Group

CONTEXT: Cirrhosis is a progressive chronic hepatopathy which constitutes an irreversible stage of liver dysfunction. OBJECTIVES: To evaluate the oxidative stress in the blood of cirrhotic rats treated with the antioxidant melatonin. METHODS: Cirrhosis was induced through inhalation of carbon tetrachloride. Liver integrity was evaluated by measuring serum enzymes, oxidative damage measured by lipoperoxidation, and antioxidant enzyme activity in erythrocytes. Lipoperoxidation, total nitrates, collagen, and histology by picrosirius staining were evaluated in the livers of these animals (n = 15), which were divided in three groups: control, carbon tetrachloride, and carbon tetrachloride + melatonin. Melatonin (20 mg/kg) was administered intraperitoneal from week 10 of carbon tetrachloride inhalation. In order to shorten the cirrhosis induction time, phenobarbital (0.3 g/L) was added to the animals' drinking water. RESULTS: A significant impairment in the liver integrity of melatonin-treated animals as compared to cirrhotic animals was observed. In rat erythrocytes and liver, lipoperoxidation was significantly increased in the cirrhotic rats as compared to controls, as measured through thiobarbituric acid reactive substances, and significantly decreased in melatonin-treated animals as compared to cirrhotic ones. In blood, a decrease in superoxide dismutase and glutathione peroxidase enzymes was detected in the cirrhotic group as compared to the control group, with increased superoxide dismutase activity when melatonin was administered. A reduction in the levels of total nitrates was detected in the hepatic tissue of the animals in the carbon tetrachloride group as compared to the control group and an increase of these levels in the carbon tetrachloride + melatonin group. As for hepatic collagen, we found a significant increase in the carbon tetrachloride group as compared to the controls and a regression of these values in the treated group. In histology, the rats in the carbon tetrachloride group showed fibrosis and formation of fibrotic nodules, characterizing liver cirrhosis; there was reduction of nodules and fibrosis in the melatonin treated group. CONCLUSION: The data allow us to suggest that the observed oxidative stress is related to the damages caused by carbon tetrachloride and that the use of melatonin can minimize these damages

scholarly journals Cytochrome P4502E1 is present in rat pancreas and is induced by chronic ethanol administration

Gut ◽  
1998 ◽  
Vol 42 (3) ◽  
pp. 426-430 ◽  
Author(s):  
I D Norton ◽  
M V Apte ◽  
P S Haber ◽  
G W McCaughan ◽  
R C Pirola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Confidence Intervals ◽  
Chronic Ethanol ◽  
Alcoholic Pancreatitis ◽  
Ethanol Administration ◽  
Mrna Levels ◽  
Rat Pancreas ◽  
Cytochrome P4502e1 ◽  
Chronic Ethanol Consumption ◽  
Chronic Ethanol Administration

Background—The mechanisms responsible for the initiation of alcoholic pancreatitis remain elusive. However, there is an increasing body of evidence that reactive oxygen species play a role in both acute and chronic pancreatitis. In the liver, cytochrome P4502E1 (CYP2E1, the inducible ethanol metabolising enzyme) is one of the proposed pathways by which ethanol induces oxidative stress.Aims—To determine whether CYP2E1 is present in the pancreas and, if so, whether it is inducible by chronic ethanol feeding.Methods—Eighteen male Sprague-Dawley rats were pair fed liquid diets with or without ethanol as 36% of energy for four weeks. CYP2E1 levels were determined by western blotting of microsomal protein from both pancreas and liver. Messenger RNA (mRNA) levels for CYP2E1 were quantified using dot blots of total pancreatic RNA.Results—CYP2E1 was found in the pancreas. Furthermore, the amount of CYP2E1 was greater in the pancreas of rats fed ethanol compared with controls (mean increase over controls 5.1-fold, 95% confidence intervals 2.4 to 7.7, p<0.02). In the liver, induction by ethanol of CYP2E1 was similar (mean increase over controls 7.9-fold, 95% confidence intervals 5.2 to 10.6, p<0.005). Pancreatic mRNA levels for CYP2E1 were similar in ethanol fed and control rats.Conclusions—CYP2E1 is present in the rat pancreas and is inducible by chronic ethanol administration. Induction of pancreatic CYP2E1 is not regulated at the mRNA level. The metabolism of ethanol via CYP2E1 may contribute to oxidative stress in the pancreas during chronic ethanol consumption.

scholarly journals Prevention by pyrazole of the effects of chronic ethanol administration on the redox states of the hepatic nicotinamide–adenine dinucleotide (phosphate) couples and on liver and brain tryptophan metabolism in the rat

1979 ◽  
Vol 184 (1) ◽  
pp. 165-168 ◽  
Author(s):  
N F Punjani ◽  
A A B Badawy ◽  
M Evans
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Chronic Administration ◽  
Chronic Ethanol ◽  
Tryptophan Metabolism ◽  
Ethanol Administration ◽  
Redox States ◽  
Chronic Effects ◽  
Chronic Ethanol Administration ◽  
Tryptophan Pyrrolase

Chronic administration of pyrazole in the diet of rats does not cause toxicity and prevents the chronic effects of ethanol on: (1) the redox states of the hepatic NAD(P) couples; (2) liver tryptophan pyrrolase activity; (3) brain tryptophan and 5-hydroxytryptamine metabolism.

Chronic ethanol administration causes oxidative stress in the rat pancreas

1998 ◽  
Vol 131 (5) ◽  
pp. 442-446 ◽  
Author(s):  
I.D. Norton ◽  
M.V. Apte ◽  
O. Lux ◽  
PS. Haber ◽  
R.C. Pirola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Rat Pancreas ◽  
Chronic Ethanol Administration

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

Sign in / Sign up

Export Citation Format

Share Document