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Free and membrane-associated fractions of protein kinase C (PKC) from rainbow trout (Onchorynchus mykiss) brain tissue were separated by hydroxylapatite chromatography and characterized kinetically. In both resting fish and in fish swum to exhaustion, approximately 40% of the total PKC activity was bound to membranes. Quantification of the three distinct hydroxylapatite chromatography peaks (PKC types gamma, beta and alpha) in cytosolic and membrane fractions revealed different isozyme distributions. The cytosolic fraction contained 21% PKC type gamma, 52% PKC type beta and 27% PKC type alpha. The membrane-associated fraction contained 23% PKC type gamma, 28% PKC type beta and 49% PKC type alpha. Kinetic characterization of the three isozymes showed that PKC type gamma was almost completely activated by Ca2+ alone whereas PKC type beta and PKC type alpha were 40% and 60% activated by Ca2+. Full activity for all enzymes was observed only in the presence of phosphatidylserine and diacylglycerol. Differences in the kinetic constants for the three isozymes were also apparent. PKC type gamma had a much lower affinity for Histone III-S when compared with PKC types beta and alpha (100 micrograms/ml as compared with 1.7 and 5.7 micrograms/ml). PKC type gamma also had a lower affinity for calcium (0.22 microM) when compared with PKC type beta (0.08 microM) and PKC type alpha (0.05 microM). PKC type alpha had a lower affinity for phosphatidylserine (8.6 micrograms/ml) when compared with PKC type gamma (0.37 microgram/ml) and PKC type beta (0.89 microgram/ml).
Biochem Mol Biol Int 1998 Feb
PMID:Protein kinase C from rainbow trout brain: identification and characterization of three isozymes. 953 May 9

The participation of hepatic glycogenolysis and gluconeogenesis to the glycemic changes promoted by exercise was investigated. For this purpose, we employed swimming rats (2.5% body weight extra load attached to the tail, at 24 degrees C) using a favorable condition to measure hepatic glycogenolysis (fed rats) and a favorable condition to measure hepatic gluconeogenesis (fasted rats). This experimental approach permits us to compare the contribution of hepatic glycogenolysis and gluconeogenesis to glucose changes for a specific schedule of exercise. The animals were investigated at rest, after 5 minutes of swimming and after swimming to exhaustion. Our results show that hepatic glycogen has a crucial role to determine hyperglycemia during exercise. In contrast, hypoglycemia developed during exercise when glycogen was depleted. However, the ability of the liver to produce glucose from L-lactate, glycerol and L-glutamine was increased during exercise. Taken together, these findings suggest that the hepatic capacity to produce glucose from gluconeogenic substrates (except for L-alanine) was increased when hepatic glycogen stores were depleted. Thus, the increased capacity to produce glucose shown by livers from exercising rats must to be an important metabolic adaptation to protect against severe hypoglycemia.
Res Commun Mol Pathol Pharmacol 1998 Nov
PMID:Changes in glycemia induced by exercise in rats: contribution of hepatic glycogenolysis and gluconeogenesis. 1010 May 3

We designed this study to determine whether the capacity of the liver to uptake ammonia and produce urea was affected by exercise (swimming at 24 degrees C with a 2.5% extra body-weight load). For this purpose, livers from sedentary rats at rest were perfused with a buffer containing increasing concentration of NH4Cl. The maximal hepatic capacity to produce urea was found at an NH4Cl concentration of 0.25 mM. Based on this finding all experiments with livers obtained from rats subject to swimming exercise were also carried out with a NH4Cl concentration of 0.25 mM. Thus, employing this concentration of ammonia, livers from sedentary and endurance trained rats, (for a period of 11 days ), that had either been resting or had been subjected to swimming exercise for 5 min or until exhaustion, were perfused in situ and ammonia uptake and urea production were measured. Clearly, both parameters were increased by exercise. However, these changes were not affected by swimming training. In addition, we demonstrate that the effect of an acute exercise on hepatic metabolism is not restricted to ammonia metabolism since livers from sedentary rats which had been subjected to swimming exercise for 5 min or until exhaustion showed higher urea production from L-glutamine. Our results also suggest that part of the changes in ureogenesis induced by exercise is mediated by cortisol (increased ammonia uptake) and part of the changes is mediated by glucagon (urea production).
Res Commun Mol Pathol Pharmacol 1998 Dec
PMID:Swimming-exercise increases the capacity of perfused rat liver to produce urea from ammonia and L-glutamine. 1034 15

Senescence of human cells has largely been studied as an in vitro phenomenon resulting from replicative exhaustion. The literature contains many studies of retinal pigment epithelium (RPE) cells which document replicative senescence. Several studies by Burke and others illustrate the relationship between donor age and replicative lifespan, the relationship between geographical location of RPE in the posterior pole and replicative lifespan, and the phenomena of altered cellular morphology and decreased culture saturation density for senescent RPE cells. Other studies have focused on the alterations of the expression of specific genes or the alteration of enzymatic activities during the senescence of RPE cells in vitro. Recently, a technique utilizing a histochemical staining procedure for beta galactosidase has been developed which identifies senescent cells. Normal beta galactosidase histochemistry which identifies the lysosomal form of the enzyme is performed at pH 4.0, while senescence-associated beta galactosidase activity is observed at pH 6.0 and is observed in the cytoplasm. We have studied the replicative senescence of human RPE cells in vitro using this procedure and have also measured the length of chromosomal telomeres to identify the aging of cultures in vitro. Our results show that RPE cultures accumulate beta galactosidase positive cells as a function of the number of population doublings and that these data correlate with the shortening of chromosomal telomeres to a functional limit observed for many human cell types at senescence. We have also recently extended this work to the development of a senescence-associated beta galactosidase procedure for observing senescent RPE cells in vivo. Basically, the same histochemical procedure is used with a post-staining bleaching step to clearly visualize staining in the RPE. Our first studies were performed on globes from Rhesus monkeys at a variety of ages from 1 year to 29 years of age. The results show the accumulation of beta galactosidase positive cells in the older monkey eyes. We have also examined several human eyes in an attempt to observe whether any relationship exists between beta galactosidase staining and age, pathology (diabetes, basal laminar deposits), and geographical location (macula vrs. periphery). These studies represent a first effort to determine if senescent RPE are present in vivo. It will be important to extend these studies so that these data might be expressed on a quantitative bases.
Mol Vis 1999 Nov 03
PMID:Senescence of the retinal pigment epithelium. 1056 57

The possible priming by D-glucose of metabolic events in islets from control rats and Goto-Kakizaki rats (GK rats) was investigated by first incubating the islets for 120 min either in the absence of any exogenous nutrient or presence of 16.7 mM D-glucose. The islets were then incubated for a second period of 120 min either at 2.8 mM or 16. 7 mM D-glucose, the hexose being now mixed with tracer amounts of D-[U-14C]glucose and D-[5-3H]glucose. In islets from control rats first incubated in the absence of exogenous nutrient the hierarchy in the 16.7 mM/2.8 mM ratio for metabolic variables was as follows: D-[U-14C]glucose oxidation > D-[5-3H]glucose utilization and D-[U-14C]glucose conversion to amino acids > D-[U-14C]glucose conversion to acidic metabolites. When the islets from control rats were first incubated in the presence of 16.7 mM D-glucose, the preferential stimulation of mitochondrial oxidative events at high hexose concentration, as documented by the increase in the paired ratio between D-[U-14C]glucose oxidation and D-[5-3H]glucose utilization, was further enhanced. The 16.7 mM/2.8 mM ratio for the conversion of D-[U-14C]glucose to amino acids, relative to that for D-[U-14C]glucose conversion to acidic metabolites, was much lower, however, after a first incubation in the presence of D-glucose, rather than in its absence, probably as a result of the progressive exhaustion of endogenous amino acids considered as transamination partners. The major differences between these results and those obtained in islets from GK rats consisted, in the latter animals, in i) higher absolute values for all metabolic fluxes, ii) lower 16.7 mM/ 2.8 mM ratios, iii) lower paired ratio between D-[U-14C]glucose oxidation and D-[5-3H]glucose utilization, and iv) absence of a priming effect of D-glucose (16.7 mM) upon such a paired ratio in the islets incubated at 16.7 mM D-glucose during the second incubation. Taken as a whole, these observations confirm that the preferential stimulation of mitochondrial oxidative events, in response to a rise in D-glucose concentration, is impaired in islets from GK rats and extend this knowledge to the priming action of D-glucose, in high concentration, on the catabolism of the hexose during a subsequent incubation.
Int J Mol Med 2000 Jun
PMID:Altered metabolic priming by D-glucose in pancreatic islets from Goto-Kakizaki rats. 1081 13

Exercise to exhaustion leads to severe metabolic, acid-base and ionic changes in fish. It has been shown that several abiotic and biotic factors can limit burst exercise performance and the recovery process in fish. This article reviews the importance of body size, temperature, fasting/starvation and training on the ability of fish to perform and recover from exhaustive exercise. It is concluded that the constraints placed on a fish prior to and following exercise reflects the large intra-specific variability in the physiological response to exercise in fish.
Comp Biochem Physiol A Mol Integr Physiol 2000 Jun
PMID:Limits to exhaustive exercise in fish. 1093 36

Lipopolysaccharide (LPS) antigenic epitopes of natural virulent and isogenic avirulent Francisella tularensis strains and other species of the Francisella genus (F. novicida, F. novicida-like, and F. philomiragia) were studied by dot and immunoblotting. Polyclonal rabbit and human sera to virulent F. tularensis strains and monoclonal antibodies to F. tularensis LPS O-side chain were used for detecting species- and genus-specific LPS epitopes. Typical virulent F. tularensis strains produce two types of S-LPS with different antigenic specificity simultaneously. Antigenic determinants of two LPS types were located in LPS O-polysaccharide but not in the core oligosaccharide. The epitopes of the first LPS type were characterized by species specificity for F. tularensis in contrast to determinants of the second LPS type, which had epitopes common with F. novicida. Cross exhaustion of human and rabbit antitularemic sera by F. tularensis and F. novicida LPS showed that F. novicida LPS molecules contained at least two epitopes--highly specific for F. novicida and common with the second type of F. tularensis LPS. The immune response of rabbits and humans to F. tularensis LPS epitopes was different in principle. Sera from rabbits immunized with vaccine and virulent F. tularensis strains contained antibodies "recognizing" antigenic epitopes of two S-LPS forms of the bacterium: type 1 species-specific (in high titers) and type 2 epitopes common with F. novicida LPS (in low titers). In addition to these, sera from patients with tularemia contain immunoglobulins to species-specific epitopes of F. novicida LPS in high titers. Experiments on avirulent mutants showed that in some cases attenuation of F. tularensis can involve loss of species-specific LPS form, while S-LPS with epitopes common with F. novicida LPS will be retained. The difference in specificity of human and rabbit antitularemic antibodies is due to individual features in the host immune system.
Mol Gen Mikrobiol Virusol 2000
PMID:[Species- and genus-specific antigenic epitopes of Francisella tularensis lipopolysaccharides]. 1097 73

We performed in vivo studies to examine the idea that cardiac work is impaired in rainbow trout (Oncorhynchus mykiss) below a certain venous PO2 threshold. We hypothesized that coronary-ligated fish, swimming continuously at a reasonably high water velocity (1.5 body lengths x s(-1)) and exposed to progressive hypoxia, would fatigue at higher venous PO2 and ambient water PO2 compared with sham-operated fish. However, we found that both the lowest venous PO2 that supported hypoxic swimming (9.9 torr for coronary-ligated fish and 11.1 torr for sham-operated fish) and the venous PO2 at fatigue (7.8 torr and 8.6 torr, respectively) were the same for coronary-ligated and sham-operated fish. Also, both groups quit swimming at the same water PO2 heart rate and hematocrit. Nevertheless, significant differences in cardiac performance did exist between the two groups. Whereas ventral aortic blood pressure (Pva) increased significantly with hypoxic swimming in sham-operated fish, there was no such increase in coronary-ligated fish. In addition, cardiac arrhythmias occurred in coronary-ligated fish at fatigue, and these fish were slower to recover from exhaustion. We believe that the venous PO2 threshold to support cardiac performance in the absence of a coronary supply was between 7.8 and 9.9 torr. Furthermore, we suspect that the low PO2 in coronary-ligated fish effectively lowered their myocardial O2 demand. Uncertainty still exists regarding whether or not the venous PO2 threshold lies between 8.6 and 11.1 torr in sham-operated fish.
Comp Biochem Physiol A Mol Integr Physiol 1998 Feb
PMID:Swimming performance, venous oxygen tension and cardiac performance of coronary-ligated rainbow trout, Oncorhynchus mykiss, exposed to progressive hypoxia. 1124 6

When protective clothing is worn that restricts evaporative heat loss, it is not valid to assume that the higher sweat rates associated with improvements in aerobic fitness will increase heat tolerance. An initial study compared thermoregulatory and cardiovascular responses to both compensable and uncompensable heat stress before and after 8 weeks of endurance training in previously sedentary males. Despite a 15% improvement in VO2peak, and lower heart rates and rectal temperature (T(re)) responses while wearing combat clothing, no changes were noted when subjects wore a protective clothing ensemble. Tolerance times were unchanged at approximately 50 min. A subsequent short-term training model that used daily 1-h exercise sessions for 2 weeks also failed to show any benefit when the protective clothing was worn in the heat. Cross-sectional comparisons between groups of high and low aerobic fitness, however, have revealed that a high aerobic fitness is associated with extended tolerance time when the protective clothing is worn. The longer tolerance time is a function of both a lower starting T(re) and a higher T(re) tolerated at exhaustion. Improvements in cardiovascular function with long-term training may allow higher core temperatures to be reached prior to exhaustion. Conversely, elevations in core temperature that occur with normal training sessions may familiarize the more fit subjects to the discomforts of exercise in the heat. Other factors such as differences in body fatness may account for a faster increase in tissue temperature at a given metabolic rate for less fit individuals.
Comp Biochem Physiol A Mol Integr Physiol 2001 Apr
PMID:The importance of aerobic fitness in determining tolerance to uncompensable heat stress. 1128 13

The aim of the present study was to ascertain the effects of training and exhaustive exercise on mitochondrial capacities to oxidize pyruvate, 2-oxoglutarate, palmitoylcarnitine, succinate and ferrocytochrome c in various tissues of the rat. Endurance capacity was significantly increased (P<0.01) by an endurance training program over a period of 5-6 weeks. The average run time to exhaustion was 214.2+/-23.8 min for trained rats in comparison with 54.5+/-11.7 min for their untrained counterparts. Oxidative capacities were reduced in liver (P<0.05) and brown adipose tissue (P<0.05) as a result of endurance training. On the contrary, the oxidative capacity of skeletal muscle was slightly increased and that of heart almost unaffected except for the oxidation of palmitoylcarnitine, which was significantly reduced (P<0.05) as a result of training.
Comp Biochem Physiol A Mol Integr Physiol 2001 Apr
PMID:The effects of endurance training and exhaustive exercise on mitochondrial enzymes in tissues of the rat (Rattus norvegicus). 1128 30


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