No increase in alcohol dehydrogenase levels following repeated ethanol exposure in young honeybee workers

2021 ◽  
Author(s):  
Krzysztof Miler ◽  
Daniel Stec ◽  
Laura Pardyak ◽  
Alicja Kamińska ◽  
Karolina Kuszewska
1985 ◽  
Vol 27 (2) ◽  
pp. 158-164 ◽  
Author(s):  
Caroline H. Wang ◽  
Shiva M. Singh

Most genetic studies on individual and racial differences in sensitivity to alcohol intoxication have concentrated on genetic variations associated with structural genes for the enzymes involved in alcohol metabolism, including alcohol dehydrogenase (ADH; E.C. 1.1.1.1). We studied the ethanol-induced regulation of ADH following chronic administration of ethanol in mice. Newly weaned males from six inbred strains (BALB/c, C3H/HeSnJ, C3H/S, C57BL/6J, S.W., and 129/ReJ) were subjected to ethanol administration. Alterations in the level of liver ADH activity, relative to matched littermate controls, were evaluated. The change in ADH activity was found to be strain (genotype) specific, which may explain the contradictory results in the literature. Strains which showed induction of ADH activity, in general, reflected a strain-specific time-dependent profile. Strains which showed repression, however, were independent in the degree of repression to the duration of ethanol exposure. Such variable, ethanol-induced regulatory responses (induction/repression) in ADH activity of different genotypes may account for individual and population variations in response to alcohol. Additional work, however, is needed to establish the molecular bases of ADH inducibility and its specific role in relative susceptibility to alcohols.Key words: alcohol dehydrogenase, mice, ethanol effects.


Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.


Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie ◽  
T.B. Cole

Ultrastructural alterations of skeletal muscle have been observed in adult chronic alcoholic patients. However, no such study has been performed on individuals prenatally exposed to ethanol. In order to determine if ethanol exposure in utero in the latter stages of muscle development was deleterious, skeletal muscle was obtained from newborn guinea pigs treated in the following manner. Six Hartly strain pregnant guinea pigs were randomly assigned to either the ethanol or the pair-intubated groups. Twice daily the 3 ethanol-treated animals were intubated with Ensure (Ross Laboratories) liquid diet containing 30% ethanol (6g/Kg pre-pregnant body weight per day) from day 35 of gestation until parturition at day 70±1 day. Serum ethanol levels were determined at 1 hour post-intubation by the Sigma alcohol test kit. For pair-intubation the Ensure diet contained sucrose substituted isocalorically for ethanol. Both food and water intake were monitored.


1986 ◽  
Vol 47 (C8) ◽  
pp. C8-1165-C8-1168
Author(s):  
M. ZEPPEZAUER ◽  
C. HAAS ◽  
W. MARET ◽  
C. HERMES ◽  
R. F. PETTIFER

2009 ◽  
Vol 47 (01) ◽  
Author(s):  
L Ciuclan ◽  
C Stump ◽  
I Ilkavets ◽  
H Weng ◽  
MV Singer ◽  
...  

2009 ◽  
Vol 47 (09) ◽  
Author(s):  
LI Ciuclan ◽  
S Ehnert ◽  
I Ilkavets ◽  
H Weng ◽  
H Gaitantzi ◽  
...  

1970 ◽  
Vol 31 (3) ◽  
pp. 571-577 ◽  
Author(s):  
Guillermo Ugarte ◽  
María Eugenia Pino ◽  
Herbert Altschiller ◽  
Tamara Pereda

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