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.

scholarly journals Enhancement of rat brain tryptophan metabolism by chronic ethanol administration and possible involvement of decreased liver tryptophan pyrrolase activity

1979 ◽  
Vol 178 (3) ◽  
pp. 575-580 ◽  
Author(s):  
A A Badawy ◽  
N F Punjani ◽  
M Evans
Keyword(s):  
Methylene Blue ◽  
Rat Brain ◽  
Chronic Ethanol ◽  
Tryptophan Metabolism ◽  
Ethanol Administration ◽  
Chronic Ethanol Administration ◽  
Tryptophan Pyrrolase ◽  
Tryptophan Concentration ◽  
Phenazine Methosulphate ◽  
The Brain

1. Chronic ethanol administration enhances rat brain 5-hydroxytryptamine synthesis by increasing the availability of circulating tryptophan to the brain. This increased availability is not insulin-mediated or lipolysis-dependent. 2. Under these conditions, tryptophan accumulates in the liver and apo-(tryptophan pyrrolase) activity is completely abolished, but could be restored by administration of regenerators of liver NAD+ and/or NADP+. 3. All four regenerators used (fructose, Methylene Blue, phenazine methosulphate and sodium pyruvate) prevented the ethanol-induced increase in liver tryptophan concentration and the increased availability of tryptophan to the brain. 4. It is suggested that the enhancement of brain tryptophan metabolism by chronic ethanol administration is caused by the decreased hepatic tryptophan pyrrolase activity. The results are briefly discussed in relation to previous work with ethanol. 5. Fructose enhances the conversion of tryptophan into 5-hydroxyindol-3-ylacetic acid in brains of ethanol-treated rats, whereas Methylene Blue inhibits this conversion in both control and ethanol-treated animals.

scholarly journals Inhibition of rat brain tryptophan metabolism by ethanol withdrawal and possible involvement of the enhanced liver tryptophan pyrrolase activity

1980 ◽  
Vol 192 (2) ◽  
pp. 449-455 ◽  
Author(s):  
A A B Badawy ◽  
N F Punjani ◽  
C M Evans ◽  
M Evans
Keyword(s):  
Rat Brain ◽  
Ethanol Withdrawal ◽  
Chronic Ethanol ◽  
Tryptophan Metabolism ◽  
Ethanol Administration ◽  
Time Intervals ◽  
Chronic Ethanol Administration ◽  
Tryptophan Pyrrolase ◽  
The Brain ◽  
Withdrawal Phase

1. Chronic ethanol administration to rats was previously shown to enhance brain 5-hydroxytryptamine synthesis by increasing the availability of circulating tryptophan to the brain secondarily to the NAD(P)H-mediated inhibition of liver tryptophan pyrrolase activity. 2. At 24h after ethanol withdrawal, all the above effects were observed because liver [NAD(P)H] was still increased. By contrast, all aspects of liver and brain tryptophan metabolism were normal at 12 days after withdrawal. 3. At 7–9 days after withdrawal, brain 5-hydroxytryptamine synthesis was decreased, as was tryptophan availability to the brain. Liver tryptophan pyrrolase activity at these time-intervals was maximally enhanced. 4. Administration of nicotinamide during the withdrawal phase not only abolished the withdrawal-induced enhancement of tryptophan pyrrolase activity on day 8, but also maintained the inhibition previously caused by ethanol. Under these conditions, the withdrawal-induced decreases in brain 5-hydroxytryptamine synthesis and tryptophan availability to the brain were abolished, and both functions were enhanced. Nicotinamide alone exerted similar effects in control rats. 5. It is suggested that ethanol withdrawal inhibits brain 5-hydroxytryptamine synthesis by decreasing tryptophan availability to the brain secondarily to the enhanced liver tryptophan pyrrolase activity. 6. The results are discussed in relation to the possible involvement of 5-hydroxytryptamine in dependence on ethanol and other drugs.

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.

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 The effects of chronic phenobarbitone administration and subsequent withdrawal on the activity of rat liver tryptophan pyrrolase and their resemblance to those of ethanol

1973 ◽  
Vol 135 (3) ◽  
pp. 555-557 ◽  
Author(s):  
Abdulla A.-B. Badawy ◽  
Myrddin Evans
Keyword(s):  
Enzyme Activity ◽  
Rat Liver ◽  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Ethanol Inhibition ◽  
Chronic Ethanol Administration ◽  
Tryptophan Pyrrolase ◽  
Subsequent Withdrawal

Chronic phenobarbitone administration inhibits the apo-(tryptophan pyrrolase) activity in homogenates of rat liver and subsequent withdrawal enhances the enzyme activity by 2.5-fold. Similar effects have been previously produced by chronic ethanol administration and withdrawal, but, whereas NADH may cause the ethanol inhibition, that by phenobarbitone may be mediated by NADPH.

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