Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.3.1 (citrate synthase)
 4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three measures of locomotory performance and a series of variables thought to affect performance were measured in the iguanid lizard Ctenosaura similis. Burst speed is mass independent; however, endurance time at 1 km/h (EN-DUR) and maximal distance run (MAX DIS) scale as M0.3. Standard and maximal rates of O2 consumption (VO2max) scale as M0.9; VO2max averages 10-fold greater than standard metabolic rate (SMR). Three of ten enzyme activities measured exhibit significant scaling. After statistically removing the effects of body mass, multiple-regression analysis indicates that 1) 89% of the residual variation in ENDUR is correlated with variation among individuals in thigh muscle mass, VO2max, heart mass, and liver citrate synthase (CS) activity; 2) maximal CO2 consumption (VCO2max) and thigh pyruvate kinase activity statistically explain 64% of the variation in MAX DIS; 3) heart and liver masses together predict 35% of the variation in SMR; 4) thigh and liver CS activity, heart lactate dehydrogenase (LDH) activity, and hematocrit account for 67% of the variation in VO2max;5) 97% of the variation in VCO2max is statistically related to variation in liver CS activity, thigh and heart masses, and heart LDH activity.
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PMID:Physiological correlates of locomotory performance in a lizard: an allometric approach. 623 43

Rats of similar mass and genetic stock have up to a 50-fold difference in spontaneous daily running distance. However, the reasons for this large variability in spontaneous running distance are not known. This study examined whether tests of running performance predict subsequent spontaneous running distance in rats housed in individual running wheel cages. Long-Evans rats (n = 56) were randomly assigned to either a sedentary control group (C) or a group housed in specially designed wheel cages in which they were able to exercise spontaneously (ES). They then underwent a high-intensity running test (MAX), during which oxygen consumption was measured at a submaximal (VO2 submax) and maximal workload (VO2 max). The rats' submaximal running endurance (END) and maximal sprinting speed (SPRINT) were also tested on the treadmill. After 8 weeks the average spontaneous running distance of ES was 29.7 +/- 3.7 km.wk-1 (mean +/- SE), but ranged from 1.4 to 71.1 km.wk-1. Tests of running performance and oxygen consumption were repeated in both groups, followed by in situ measurements of muscle contractile properties and of citrate synthase activity in the skeletal muscle. None of the measurements of running performance or oxygen consumption during the initial tests conducted at the start of the experiment was related to subsequent average spontaneous running distance. After 8 weeks, the mean peak force generated by the electrically stimulated gastrocnemius/plantaris muscles was greater in ES than in C (746 +/- 89 vs. 455 +/- 28 mg, p < 0.005), but this difference was not related to spontaneous running distance. Conversely, citrate synthase activity of the soleus muscle after training was related to average spontaneous running distance (r = 0.92, p < 0.0004). Average spontaneous running distance was also related to MAX (r = 0.65, p < 0.002), END (r = 0.59, p < 0.0009), and SPRINT (r = 0.61, p < 0.0005) and was inversely related to running intensity (r = -0.66, p < 0.002) after 8 weeks of training. It can be concluded from this study that 1) spontaneous running distance in rats cannot be predicted by pretraining tests of running performance. Hence, low levels of spontaneous running activity in some rats are not explained by skeletal muscular and cardiovascular factors thought to determine running capacity, and 2) posttraining tests of running performance were proportionally related to total spontaneous running distance and muscle oxidative enzyme changes but not to the in situ contractile properties of the muscles.
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PMID:Tests of running performance do not predict subsequent spontaneous running in rats. 880 59

To date, the consequences of succinate dehydrogenase (SDH) impairment on overall mitochondrial functions are still obscure. In this study, we evaluated SDH activity and expression and mitochondrial homeostasis in 57 tissue samples of pheochromocytoma (PHEO)/paraganglioma (PGL) obtained from patients genotyped for PHEO/PGL susceptibility genes. The resulted SDH activity and content always decreased in SDH-mutated tumors, in one out of two MAX-mutated patients and in four patients resulted wild type (wt) at genetic screening. All these four wt patients were further screened for large deletions in SDH genes, TMEM127 and MAX and resulted wt but two had somatic SDHD mutations. The RT-PCR in the MAX-mutated sample suggests that the decrease in SDH depends on complex instability and not on a reduced SDHB expression. SDH mutations neither alter citrate synthase (CS) activity nor the content of voltage-dependent anion channel (VDAC) while the expression of the mitochondrial complex IV (cytochrome c oxidase (COX)) was found extremely variable in all (mutated and wt) samples suggesting an impairment of mitochondrial cristae in these tumors. In conclusion, tumors from patients with germ line SDH mutations invariably show decreased enzymatic activity and content, but an SDH impairment may also depend on SDH somatic mutations or, seemingly, on MAX mutations. The impaired SDH activity in the two wt tissues suggests mutations in other still unknown susceptibility genes. Finally, the extreme variability in COX expression levels is yet to be explained and this strongly suggests to evaluate other mitochondrial features to better understand the mitochondrial role in the pathogenesis of these tumors.
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PMID:Mitochondrial function and content in pheochromocytoma/paraganglioma of succinate dehydrogenase mutation carriers. 2232 61