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GSH, and T-AOC were significantly decreased by isoproterenol administration, while
myocardial MDA was significantly increased. Besides results presented in Fig. 21.3
also denote that isoproterenol administration increased slightly activities of antioxi-
dant enzymes in myocardium such as SOD and GSH, which indicate that oxidative
stress caused by isoproterenol may upregulate the activity of antioxidant enzymes in
myocardium to facilitate rapid removal of the accumulated reactive oxygen species.
GSH is one of the most important compounds, which helps in the detoxification and
excretion of oxygen radicals. SOD is the first line of defense against ROS; as a metal-
loprotein, its antioxidant functions were exhibited by enzymatically detoxifying the
peroxides and superoxide anion. MDA as a breakdown product from oxidation reac-
tions of polyunsaturated fatty acids, the level of MDA can be taken as an indicator for
the state of lipid peroxidation. Gan et al. ( 2006 ) have suggested that MDA can be as
the one of the major indicators of free radical-mediated tissue injury. T-AOC which is
an indicator of body antioxidant ability could indicate the compensatory ability of
antioxidase system and nonenzymatic system to stimuli.
The present results showed the levels of GSH and T-AOC in myocardium, and
the levels of serum SOD, GSH-Px, GSH, and T-AOC were significantly increased,
but the MDA in myocardium and serum was significantly decreased by administra-
tion of taurine compared with model group. Taurine is an important endogenous
antioxidant; many studies have demonstrated that taurine exhibits a protective action
under oxidative stress condition (Oudit et al. 2004 ; Chang et al. 2004 ; Shiny et al.
2005 ; Schaffer et al. 2009 ; Yang et al. 2010 ). The possible mechanisms for taurine
protective actions include a direct effect as a free radical scavenger, or indirectly,
preventing generation of reactive oxygen species and/or protecting cell membranes
from ROS damage (Schaffer et al. 2009 ). In the study, we also found that taurine
was apparently beneficial for the ISO-induced myocardial injury in rats, decreasing
MDA formation and augmenting the antioxidative enzymes activities. This was
consistent with Shi et al. ( 2002 ) .
The results indicated that taurine can not only improve the myocardium oxida-
tive stability but also obviously improve serum oxidative stability, decrease lipid
peroxidation, and strengthen the myocardial membrane. Previous research has sug-
gested that except fox and cat, the size of the intracellular taurine pool of most ani-
mal species remains fairly constant even with significant reductions in dietary
taurine content, which was caused by the decline in plasma taurine levels accompa-
nied by enhanced cellular retention of taurine (Hamaguchi et al. 1991 ) . On the other
hand, research has suggested taurine levels were increased under some conditions,
such as failing and hypertrophic heart (Huxtable and Bressler 1974 ) . This is the
reason why the taurine increases the serum oxidative stability more obviously.
Myocardial ultrastructure observations showed that taurine is capable of not only
obviously inhibiting myofibrillar disruption but also enhancing the integrity of mito-
chondrial membranes and cristae; the results indicated administration of 200 mg/kg
taurine has better protective effect. It had been reported that downregulation of the
taurine gene leads to lost cell volume, develops mitochondrial defects, and undergoes
myofibrillar disruption (Ito et al. 2008 ). The results are consistent with the action of
taurine as an osmoregulator, mitochondrial modulator, and a cytoprotective agent.
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