Biology Reference
In-Depth Information
a
b
1000
1000
Control
2% Tau
T+CTM
**
**
**
**
**
**
*
*
**
**
**
**
**
**
**
900
900
*
*
**
**
**
**
**
*
*
*
*
*
*
*
*
800
*
*
*
*
*
*
*
*
**
**
**
**
**
**
*
*
*
*
*
*
*
*
**
**
**
**
**
700
800
*
*
*
*
*
*
*
*
*
*
**
**
**
**
**
*
*
*
*
*
*
*
*
600
*
*
*
*
*
*
*
*
**
**
**
**
**
**
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
700
500
400
300
200
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
600
500
20
50
90
120
150
20
50
90
120
150
Fig. 3.3
(
a
) Hepatic activity of ADH. (
b
) Hepatic activity of ALDH. Mice in the control, 2% Tau,
and T+CTM groups were administered with water, 2% taurine, or 2% taurine coadministration
with Chinese traditional medicine, respectively, 30 min before alcohol intake. Liver were collected
20, 50, 90, 120, and 150 min after alcohol intake. Each column and vertical bar represents the
mean ± SEM. Values with asterisk are significantly different (
P
< 0.05), values with double asterisks
are very significantly different (
P
< 0.01 ANOVA followed by the Tukey's post hoc test)
3.4
Discussion
It is now clear that acute alcohol binges is not only toxic to the liver but also can
contribute to the chronicity of ALD. Potential mechanisms by which acute alcohol
causes damage include steatosis, dysregulated immunity and inflammation, and
altered gut permeability (Massey and Arteel
2012
). Ethanol is mainly metabolized in
the liver by two oxidative pathways. In the first pathway, ethanol is oxidized to
acetaldehyde by the cytoplasmic ADH enzyme, and acetaldehyde is then oxidized to
acetic acid by the mitochondrial ALDH. The second pathway is inducible and
involves the microsomal ethanol-oxidizing system (MEOS), in which the oxidation
of ethanol to acetaldehyde and acetic acid also leads to generation of reactive oxygen
species (ROS). Chronic or acute ethanol consumption significantly inhibits mito-
chondrial ADH and ALDH activity, resulting in a striking increase of tissue and
blood alcohol and acetaldehyde levels (Lieber
1997
) .
The main enzyme for taurine synthesis is mainly distributed in the liver, which is
considered to be the main organ capable of taurine synthesis, suggesting that taurine
may play vital roles in the liver protection. We have also previously found that
taurine had significant protective effects on alcoholic liver disease (Wu et al.
2009
) .
Many Chinese traditional medicines which were used in the present research have
been reported to have hepatoprotective effects such as radix bupleuri, fructus aurantii,
and Salvia and Chrysanthemum flowers (MingHong Yen et al.
2005
, Lihua Liu
et al.
2009
, Tetuya Sugavara and Kiharu Igarashi
2009
) . Moreover, fl ower of
kudzuvine has been reported to accelerate the metabolism of alcohol (Ping Li and
Gansheng Zhong
2009
) .
In the present study, blood alcohol concentration increased obviously in the
control group, and arrived at the highest point 90 min after alcohol intake. Taurine
group showed a slightly increase and the highest point was at 50 min after alcohol
intake. While in T+CTM group, blood concentration began to decrease 20 min after
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