Liver Tryptophan Pyrrolase and Brain 5-Hydroxytryptamine: Effects of Chronic Ethanol Administration

1978 ◽  
Vol 6 (5) ◽  
pp. 1002-1004 ◽  
Author(s):  
ABDULLA A.-B. BADAWY ◽  
NAZEERA F. PUNJANI ◽  
MYRDDIN EVANS
Keyword(s):  
Chronic Ethanol ◽  
Ethanol Administration ◽  
Chronic Ethanol Administration ◽  
Tryptophan Pyrrolase

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 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 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 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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