scholarly journals The protective effect of L-glutamine against acute Cantharidin-induced Cardiotoxicity in the mice

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Haozhen Shao ◽  
Lei Dong ◽  
Yanyan Feng ◽  
Chunhui Wang ◽  
Hongxuan Tong
Keyword(s):  
Protective Effect ◽  
Succinate Dehydrogenase ◽  
Dehydrogenase Activity ◽  
Biological Markers ◽  
Control Group ◽  
Protective Mechanism ◽  
High Dose ◽  
Severe Toxicity ◽  
Antitumor Effects ◽  
Succinate Dehydrogenase Activity

Abstract Background Cantharidin (CTD) is a compound which have the potential to be exploited as an antitumor drug, and it has been demonstrated antitumor effects in a variety of cancers. However, the use is limited due to its severe toxicity. It has reported that it can induce fatal cardiac arrhythmias. Fortunately, we found that L-glutamine can alleviate cardiac toxicity caused by cantharidin in mice. Methods To investigate the protective effect of L-glutamine, we used a high dose of cantharidin in mice to create a model of cardiotoxicity. In the experimental mice, glutamine was given orally half an hour before they were administrated with cantharidin. The mice of control group were intraperitoneally injected with DMSO solution. The general state of all mice, cardiac mass index, electrocardiogram change and biological markers were determined. Hematoxylin-eosin staining (HE staining) of heart tissue was carried out in each group to reflect the protective effect of glutamine. To investigate the mechanisms underlying the injury and cardio-protection, multiple oxidative stress indexes were determined and succinate dehydrogenase activity was evaluated. Result The results showed that L-glutamine (Gln) pretreatment reduced weight loss and mortality. It also decreased the biological markers (p < 0.05), improved electrocardiogram and histological changes that CTD induced cardiotoxicity in mice. Subsequently, the group pretreated with L-glutamine before CTD treatment increases in MDA but decreases in SOD and GSH, in comparison to the group treated with CTD alone. Besides, succinate dehydrogenase activity also was improved when L-glutamine was administrated before cantharidin compared to cantharidin. Conclusions This study provided evidence that L-glutamine could protect cardiac cells against the acute cantharidin-induced cardiotoxicity and the protective mechanism of glutamine may be related to the myocardial cell membrane or the tricarboxylic acid cycle in the mitochondria.

Interactive effects of emphysema and malnutrition on diaphragm structure and function

1994 ◽  
Vol 77 (2) ◽  
pp. 947-955 ◽  
Author(s):  
M. I. Lewis ◽  
S. A. Monn ◽  
W. Z. Zhan ◽  
G. C. Sieck
Keyword(s):  
Succinate Dehydrogenase ◽  
Dehydrogenase Activity ◽  
Cross Sectional Area ◽  
Interactive Effects ◽  
Type I ◽  
Specific Force ◽  
Type Ii ◽  
Sectional Area ◽  
Succinate Dehydrogenase Activity ◽  
Cross Sectional

Interactive effects of emphysema (EMP) and prolonged nutritional deprivation (ND) on contractile, morphometric, and metabolic properties of hamster diaphragm muscle (DIA) were examined. Six months after induction of EMP (intratracheal elastase), saline-treated controls (CTL) and EMP hamsters of similar body weights were subjected to ND over 6 wk. Isometric contractile and fatigue properties of costal DIA were determined in vitro. DIA fibers were histochemically classified as type I or II, and fiber succinate dehydrogenase activity and cross-sectional area were determined using quantitative microscopic procedures. From histochemical sections, the number of capillaries per fiber (C/F) and per fiber cross-sectional area (C/A) were determined. ND resulted in progressive loss of body weight (ND-CTL, 23.8%; ND-EMP, 28.4%; P = NS). ND did not affect reduction in optimal length (Lo) of DIA fibers in EMP compared with CTL and ND-CTL hamsters. Maximum specific force (i.e., force/unit area) was reduced by approximately 25% in EMP animals compared with CTL. ND did not improve or exacerbate the reduction in specific force with EMP. ND attenuated improved fatigue resistance of DIA in EMP animals. No differences in fiber type proportions were noted among experimental groups. Significant atrophy of type I and II DIA fibers was noted after ND. Atrophy was proportionately greater in type II fibers of ND-EMP when referenced to EMP animals. Thus adaptive hypertrophy of type II DIA fibers in EMP animals was abolished. Fiber succinate dehydrogenase activity was significantly increased in type I and II fibers in EMP DIA. ND did not affect this metabolic adaptation of DIA fibers to persistent loads imposed by EMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracellular distribution of succinate dehydrogenase activity in skeletal muscle fibers of geese

1984 ◽  
Vol 62 (2) ◽  
pp. 235-240 ◽  
Author(s):  
H. J. Swatland
Keyword(s):  
Skeletal Muscle ◽  
Succinate Dehydrogenase ◽  
Dehydrogenase Activity ◽  
Adenosine Triphosphatase ◽  
Muscle Fibers ◽  
Fiber Types ◽  
Succinate Dehydrogenase Activity ◽  
Individual Muscle ◽  
Concentric Zone ◽  
Pectoralis Muscles

Samples of iliotibialis anterior and pectoralis muscles were taken from five ganders (Anser domesticus). Serial transverse sections were reacted for succinate dehydrogenase (SDH) and alkali-stable adenosine triphosphatase (ATPase). The distribution of SDH activity within individual muscle fibers was measured with a scanning photometer. In many individual fibers, SDH activity was stronger in the periphery than in the axis. This gradient was steepest (−0.034 ± 0.019 absorbance units per concentric zone of 2 μm diameter measurements) in pectoralis fibers with strong SDH activity. In the pectoralis, radial gradients were correlated with fiber area so that the smallest fibers tended to have the steepest gradients of SDH activity. However, this relationship was reversed in fibers with strong ATPase and weak SDH activity in the iliotibialis anterior, and the largest fibers tended to have the steepest gradients. In all fiber types of both muscles, fibers with greater mean SDH activity tended to have steeper gradients.

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