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Biomedical subjects

J A Sturman

Publications and source records attributed to J A Sturman.

At least 19 recordsLinked to original sources
PubMed1992

"Activation" of alveolar leukocytes isolated from cats fed taurine-free diets.

Taurine is a ubiquitous amino sulfonic acid in mammals, present in high concentrations in tissues, including those exposed to elevated levels of oxidants. Experiments were designed to examine the consequences of taurine deficiency on production of ROI in leukocytes isolated from the lungs and blood of cats fed taurine-deficient diets. Cats were maintained on taurine-free or taurine-supplemented diets for at least 12 months at which time taurine deficiency was evident. To analyze alveolar cells, lungs were lavaged to recover lung macrophages and PMNs. Lung lavage fluid from cats contained macrophages and PMNs, although taurine deficiency was associated with a decrease in the percentage of PMNs in the lungs. This is similar to our findings in blood that taurine deficiency reduced the proportion of PMNs. Taurine measurements revealed 2.1 +/- 1.6 mumol/g wet wt of taurine in the lungs from cats fed a taurine-deficient diet versus 8.3 +/- 2.6 in lungs from cats fed a diet supplemented with taurine (n = 16). The effects of taurine deficiency on the functional activity of lung macrophages and PMNs were analyzed including the production of ROI. Alveolar leukocytes from cats fed taurine-deficient diets produced more superoxide anion in response to phorbol myristate acetate than cats fed taurine supplemented diets. Similar results were obtained using a chemiluminescence assay. Using the highly specific H2O2 indicator dye, dichlorofluorescin, and flow cytometry we found that alveolar leukocytes made more H2O2 than cells from cats fed taurine-supplemented diets. Forty-two percent of the cells from cats fed a taurine-supplemented diet expressed class II antigens. In contrast, 72% of cells from the taurine-deficient cats expressed this antigen. We hypothesize that taurine functions to prevent terminal activation and release of cytotoxic mediators by lung macrophages. Thus, a deficiency of taurine will indeed cause an activation of leukocytes, as evidenced by our data which show an increase in ROI, as well as an increase in class II antigen.

Amino Acids↗
PubMed1992

High dietary taurine effects on feline tissue taurine concentrations and reproductive performance.

The reproductive performance and outcome of kittens was determined for female cats fed 0.05, 0.2 or 1% taurine. No adverse effects of high taurine diets were noted in the adults or offspring, and the reproductive performance was slightly better than that of females fed the normal (0.05% taurine) diet. Body weight at birth and brain weight at weaning were significantly greater in the very high taurine group than in the normal taurine group, although the greatest growth rate was achieved by the normal taurine group. The concentration of taurine in milk of lactating females was substantially higher in cats fed the higher taurine diets. Brain of adult cats was resistant to increases in brain taurine concentrations, as was brain of newborn cats. However, brain of juvenile cats responded to higher dietary taurine intake with increased taurine concentrations. These results indicate that the higher taurine content in cat foods recently introduced for prevention of feline dilated cardiomyopathy should have no adverse effects over a prolonged period on health and reproduction of cats.

Administration, Oral↗
PubMed1992

Taurine attenuates renal disease in chronic puromycin aminonucleoside nephropathy.

Repeated administration of low doses of puromycin aminonucleoside (PAMN) to rats induces a proteinuric renal disease that resembles focal segmental glomerulosclerosis (FSGS). Reactive oxygen molecules may be involved in the progressive course of this nephropathy. Therefore we evaluated whether taurine, an endogenous antioxidant, could limit the extent of renal injury. Sprague-Dawley rats received low-dose injections of PAMN, 2 mg/100 g body wt, over a 12-wk period. Two groups were studied: 1) controls given tap water (n = 23), and 2) an experimental group that drank 1% taurine-supplemented water (n = 22). Taurine-treated nephrotic rats had a reduction in albuminuria, as assessed by the urinary albumin-to-creatinine ratio (26 +/- 4 vs. 44 +/- 4, P less than 0.0001). After 12 wk, creatinine clearance was 0.33 +/- 0.03 (experimental) vs. 0.17 +/- 0.03 ml.min-1.100 g body wt-1 (control) (P less than 0.001), and inulin clearance (n = 6 pairs) was 0.26 +/- 0.04 (experimental) vs. 0.13 +/- 0.02 ml.min-1.100 g body wt-1 (control) (P less than 0.025). Administration of taurine reduced the percentage of segmentally sclerosed glomeruli (9.8 +/- 1.7 vs. 16.2 +/- 1.8%, P less than 0.02) and the tubulointerstitial injury score (1.36 +/- 0.19 vs. 2.61 +/- 0.25, P less than 0.0025) in experimental vs. control rats. Taurine treatment normalized the elevated renal cortical malondialdehyde level in rats with PAMN nephropathy (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Cerebral taurine transport is increased during streptozocin-induced diabetes in rats.

Taurine is a cerebral osmolyte whose intracellular content changes in parallel with plasma osmolality. We conducted experiments to assess whether cerebral taurine transport is modified during chronic hyperglycemia. Rats with STZ-induced diabetes were studied after 1 wk of sustained hyperglycemia. Cerebral taurine uptake in synaptosomes (metabolically active nerve terminal vesicles) was measured using a rapid filtration technique. The synaptosomes were isolated by homogenization of the brain and purification on discontinuous Ficoll gradients (n = 8 synaptosome preparations). Diabetic rats (n = 13) displayed a 15-25% increase in synaptosomal taurine uptake compared with normoglycemic control animals (n = 12) at all time points assayed between 5 and 120 min. Thus, after a 30-min incubation, cerebral taurine uptake increased from a control level of 3.53 +/- 0.23 to 4.10 +/- 0.24 mumol/mg protein (n = 10) in hyperglycemic rats, P less than 0.03. The magnitude of the plasma-to-brain cell taurine gradient was unchanged in diabetic animals. The intrasynaptosomal taurine concentration (approximately 2 microM) and taurine efflux from the synaptosomes were no different in hyperglycemic versus control rats; efflux amounted to less than 2.5% of the uptake value at corresponding time points. Maximal brain taurine uptake under both control and experimental hyperglycemic conditions required the presence of external Na+ and Cl-. Synaptosomal taurine transport was reduced by competing beta-amino acids such as beta-alanine, beta-aminoisobutyric acid, and hypotaurine (P less than 0.01). Addition of oubain and the anionic binding site inhibitors, 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid and 4,4'diisothio-cyanatostilbene-2,2'-disulfonic acid, also decreased cerebral taurine uptake under normoglycemic and hyperglycemic conditions (P less than 0.01). The increased synaptosomal taurine uptake by diabetic rats was not a result of generalized membrane dysfunction because glycine transport was not elevated in hyperglycemic rats. The enhanced transport rate was attributable to a 35 and 81% increase in the Vmax of the high- and low-affinity taurine transporters, respectively (P less than 0.01), without significant change in the Km of the carrier systems. Treatment of hyperglycemic rats (n = 5) with ultra-long-acting insulin to normalize the serum glucose concentration restored synaptosomal taurine uptake to the level observed in normoglycemic controls. The effect of insulin was attributable to correction of hyperglycemia, because addition of insulin (500 mU/ml) to the in vitro assay system did not alter synaptosomal taurine uptake.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Myocardial taurine concentrations in cats with cardiac disease and in healthy cats fed taurine-modified diets.

Myocardial taurine concentrations were measured in cats with cardiac disease and in healthy cats fed diets with various concentrations of taurine. Group 1 was composed of 26 cats with 3 categories of naturally developing cardiac disease: dilatative cardiomyopathy (group 1A), 10 cats; hypertrophic cardiomyopathy (group 1B), 9 cats; and volume overload (group 1C), 7 cats. These cats had been fed various commercial diets. Group 2 was composed of 40 healthy cats that had been fed diets varying in taurine concentration (0 to 1% taurine) for at least 2 years. Mean myocardial taurine concentrations did not differ significantly between group-1 cats with dilatative cardiomyopathy and those with hypertrophic cardiomyopathy or volume overload. Cats in group 1A had a mean myocardial taurine concentration 3 times higher than healthy cats fed a taurine-free diet (P less than 0.002). Mean myocardial taurine concentrations did not differ significantly between group-1A cats and healthy cats fed a diet containing 0.02% taurine; group-1A cats had significantly lower mean myocardial taurine concentrations than did healthy cats fed a synthetic diet containing 0.05 or 1.0% taurine (P less than 0.001). Acute oral administration of taurine in 5 group-1A cats appeared to increase mean myocardial taurine concentrations, compared with similar cats not given taurine during treatment for cardiac failure. In group-2 cats, mean myocardial taurine concentrations increased directly with percentage of dietary taurine.

Animals↗
PubMed1991

Comparison of the developmental changes of the brainstem auditory evoked response (BAER) in taurine-supplemented and taurine-deficient kittens.

A similar development of the brainstem auditory evoked response is present in taurine-supplemented and taurine-deficient kittens between the second postnatal week and the third month of life. Between birth and the second postnatal week kittens from mothers fed the 1% taurine diet showed earlier maturation of the brainstem auditory evoked response as indicated by lower threshold, shorter P1 latency and shorter central conduction time when compared to the kittens from mothers fed the 0.05% taurine diet. These results suggest an important role of taurine in the anatomical and functional development of the auditory system.

Acoustic Stimulation↗
PubMed1991

Distribution of taurine-like immunoreactivity in cerebellum of kittens from taurine-supplemented and taurine-deficient mothers.

Using an antibody prepared against taurine conjugated to bovine serum albumin with glutaraldehyde, the distribution of taurine in cerebellum of newborn and 8-week-old kittens from mothers fed 0, 0.02, 0.05, or 1% dietary taurine has been determined. In general, taurine-like immunoreactivity was greater in kittens from mothers fed the greatest amounts of taurine, as was the total cerebellar taurine concentration. The most notable feature in newborn kitten cerebellum was a dense band of staining in the inner molecular layer adjacent to the Purkinje cell layer, which corresponds to the short Purkinje cell dendrites. In cerebellum of 8-week-old kittens, taurine-like immunoreactivity was present in Purkinje cells and their dendrites, most granule cells, and a few interneurons in the molecular layer of the 0.02, 0.05, and 1% groups. The cerebellum of the 0% group was distinctive in that virtually no neurons were reactive, appearing as 'ghosts' against the background, and both white matter and the granule cell layer contained large numbers of reactive astrocytes. The presence of such large numbers of reactive astrocytes and the immunoglobulin within the brain suggests an impairment of the blood-brain barrier in such taurine-deficient kittens.

Animals↗
PubMed1991

The role of taurine in the survival and function of cerebellar cells in cultures of early postnatal cat.

The role of taurine and beta-alanine was analyzed in kitten cerebellar cultures. Since in contrast to mouse, cats (and primates including man) cannot synthesize sufficient taurine to maintain their body pools, we considered the cat an ideal species for the analysis of the role of taurine during early postnatal cerebellar development under controlled conditions. Unexpectedly, we found that the presence of taurine was toxic to neurons but that compounds, considered to be competitors for the beta-amino acid uptake system, support cell survival and cell function in vitro, the opposite of the results found in mice. This could be explained by the finding that only minute amounts of [3H]taurine were taken up by both cat neurons and glial cells under optimal culture conditions but that in the presence of the taurine analogues beta-alanine and guanidinoethane sulfonic acid (GES) significant amounts of taurine were found in all cell types. These differences between mouse cerebellar cells and cat cerebellar cells in vitro suggest that a re-evaluation of the mechanisms that control taurine function in cats and primates is warranted.

Animals↗
PubMed1991

Dietary taurine content changes liver lipids in cats.

Adult female cats were fed a completely defined purified diet (taurine-free) alone or containing 0.05% taurine (the normal dietary requirement) or 1% taurine (20-fold the normal dietary requirement) for greater than 2 y. The relative composition of conjugated biliary bile acids was not different among the three groups and virtually all bile acids were conjugated with taurine. The taurine concentration in liver varied dramatically with the amount of taurine in the diet. Total liver lipid content decreased with increasing dietary taurine. Individual lipid components also varied, especially free fatty acids (which decreased with increasing dietary taurine) and triglycerides (which increased with increasing dietary taurine), indicating that taurine has a metabolic effect on lipid metabolism. Taurine deficiency also caused significant changes in the fatty acid distribution of sphingomyelin. In particular, a decrease of lignoceric acid and an increase of nervonic acid were observed. The present data suggest that hepatocellular levels of taurine can modulate the mobilization of liver lipid stores and the utilization by the liver of circulating free fatty acids. These effects are probably mediated by factors affecting membrane fluidity, such as the ratio of cholesterol to phospholipids, the degree of unsaturation of phospholipids and the changes in sphingomyelin fatty acid composition.

Administration, Oral↗
PubMed1991

Tissue taurine content, activity of taurine synthesis enzymes and conjugated bile acid composition of taurine-deprived and taurine-supplemented rhesus monkey infants at 6 and 12 mo of age.

Concentrations of taurine were measured in a number of tissues from rhesus monkeys fed a taurine-free human infant formula with or without taurine supplementation for 6 mo and 12 mo. At 6 mo, tissue taurine content was significantly greater in the monkeys supplemented with taurine, but by 12 mo, there was no longer a significant difference. Activities of enzymes involved in taurine biosynthesis did not differ between the groups at any age. There was no difference in biliary bile acid class composition between the groups, but the proportion of bile acids conjugated with taurine reflected the tissue taurine content (i.e., was significantly greater in monkeys supplemented with taurine at 6 mo). This difference also disappeared by 12 mo. These results indicate that dependence on dietary sources of taurine persists for at least the first 6 mo but declines by 12 mo. Thus, dietary taurine content is reflected in the tissue taurine content and proportion of bile acids conjugated with taurine in infant rhesus monkeys at least until 6 mo of age, but the body taurine status in animals 12 mo old or older is not an indicator of previous status.

Animal Nutritional Physiological Phenomena↗
PubMed1991

Dietary taurine content and feline reproduction and outcome.

The reproductive performance and the outcome of the kittens was determined for female cats fed 0, 0.01, 0.02 or 0.05% taurine. Reproductive performance and outcome in the 0.02% group was substantially better than in the 0 and 0.01% groups but not as good as in the 0.05% group. Kittens in the 0.05% group had higher body weights and brain weights at birth and at 8 wk after birth than did kittens in the other groups. The concentration of taurine in milk was much higher in females fed 0.05% taurine (approximately 1.9 mmol/L) compared with females fed 0.02% taurine (approximately 0.55 mmol/L) or females fed 0 or 0.01% taurine (approximately 0.2 mmol/L). The concentration of taurine in tissues and fluids of adult females, newborn kittens and 8-wk-old kittens in the 0.05% group was significantly higher than in all other groups. In general, the concentration of taurine in tissues and fluids of the 0.02% group were not significantly different than in the 0 or 0.01% groups, with the exception of 8-wk-old kittens, in which several values, including retina and five brain regions, were significantly higher than in the 0 and 0.01% groups. These results indicate that the postnatal supply of taurine in the mother's milk had a greater impact than the intrauterine environment on the taurine concentration of the offspring in the 0.02% group; this amount of dietary taurine is still insufficient for a normal reproductive performance and resulted in significantly smaller taurine concentrations in adults and offspring.

Animals↗
PubMed1991

Dietary taurine and feline reproduction and development.

The reproductive performance of female cats is severely affected by dietary taurine deficiency resulting in excessive reproductive wastage, including frequently resorbed or aborted fetuses and stillborn or low birth-weight live kittens. These studies were performed using female cats fed a completely defined purified diet (taurine-free) alone or supplemented with taurine for greater than or equal to 6 mo before mating, and their breeding performance was monitored for several years. Diets containing 0, 0.005 or 0.01% taurine produced severe taurine depletion and poor reproductive performance. Those containing 0.05, 0.2 or 1% taurine resulted in no apparent abnormalities and a normal breeding performance. A diet containing 0.02% taurine resulted in no apparent abnormalities and a normal breeding performance. A diet containing 0.02% taurine resulted in modest taurine depletion and a partially compromised reproductive performance. Kittens from taurine-deficient mothers have a poor survival rate and grow at a slower rate than kittens from females fed an adequate taurine diet. The brain weights of kittens from taurine-deficient mothers are significantly smaller than normal, both at birth and at weaning at 8 wk. Surviving kittens exhibit a number of abnormalities. The differences in maternal dietary taurine are reflected in the taurine concentrations found in the milk of lactating females. Our results strongly suggest that a certain amount of taurine is mandatory for survival and normal development in the cat.

Abortion, Veterinary↗
PubMed1991

Proteins isolated from regenerating sciatic nerves of rats form aggregates following posttranslational amino acid modification.

Soluble proteins of regenerating sciatic nerves of rats can be posttranslationally, covalently modified by a variety of radioactive amino acids. The present study shows that once modified by a mixture of 15 amino acids, many of those proteins form aggregates that are unable to pass through a 0.45-micron filter and pellet following 20,000g centrifugation (suggesting a size of greater than 2 x 10(6) Da). Aggregation of proteins also occurs following modification by Arg or Lys alone, but does not occur following protein modification in nonregenerating nerves or in brain. Aggregates are not disrupted by treatment with 100 mM beta mercaptoethanol or by exposure to 1.0 M NaCl, but aggregates are solubilized by treatment with urea and by boiling in 1.5% SDS. Amino acid analysis of proteins modified by a mixture of [3H]amino acids shows a similar proportion of posttranslationally incorporated Ser, Pro, Val, Ala, Leu, Phe, Lys, and Arg in the soluble and pelletable fractions. Two-dimensional PAGE profiles of soluble and pelletable modified proteins show that the modified proteins in both fractions are in similar pI and molecular weight ranges, except that the soluble modified proteins include a high-molecular-weight component that is absent in the pelleted modified proteins. Kinetic studies show that while half-maximal levels of protein modification occur within 30 seconds of incubation, the appearance of the pelletable modified protein fraction is delayed significantly. These results indicate that amino acid modification of soluble proteins in regenerating sciatic nerves of rats results in physical changes in those proteins so that they form high-molecular-weight aggregates.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1990

The site of amino acid addition to posttranslationally modified proteins of regenerating rat sciatic nerves.

The posttranslational modification of proteins by amino acids has been described in a variety of biological systems. These reactions occur at low levels in intact sciatic nerves of rats but are increased 10-fold following nerve injury and during subsequent regeneration of the nerve. While it has been shown in brain and liver that the site of addition of Arg is to the N-terminus, there is no information on the location at which the other amino acids add on to targeted proteins nor the site of addition of Arg in regenerating nerves. In the present study, we have used manual micro-Edman degradation combined with HPLC, and digestion with carboxypeptidase A and B to determine the site of addition of various amino acids to targeted proteins. Of the 3H-labelled amino acids incorporated posttranslationally into proteins of regenerating sciatic nerves (Arg, Lys, Leu, Phe, Val, Ala, Pro and Ser), only [3H]Arg was found to be present at the N-terminus. To determine whether amino acid additions were occurring at the C-terminus, proteins modified by two of the amino acids incorporated in greatest amounts (Lys and Leu) were incubated with specific carboxypeptidases. [3H]Leucine was not liberated following incubation with carboxypeptidase, suggesting that Leu is not added at the C-terminus of modified proteins. Under similar conditions, some [3H]Lys was liberated, but in amounts not significantly different from controls incubated without carboxypeptidase, indicating a non-specific degradation of Lys modified proteins rather than a specific release of Lys from the C-terminus. These experiments show that in regenerating sciatic nerves of rats, Arg is the only amino acid added posttranslationally to the amino terminus of target proteins, and that Leu, and probably Lys, are not conjugated to proteins at the C-terminus.

Amino Acids↗
PubMed1990

Amino acid modification of proteins in regenerating sciatic nerves of rats.

Recent experiments have shown that Arg, Lys, and Leu can be incorporated posttranslationally into proteins of regenerating sciatic nerves of rats. The present experiments investigate a mixture of 15 radioactive amino acids to determine if additional amino acids can be conjugated posttranslationally to proteins of regenerating nerves. Proteins of regenerating sciatic nerves of rats were able to incorporate Arg, Lys, Leu, Pro, Val, Ala, Phe, and Ser in relatively large amounts and Asp, Glu, Thr, Gly, Ile, His, and Tyr in relatively low or undetectable amounts, in the most advanced portion of the regenerating nerves. Two-dimensional SDS PAGE showed incorporation of the amino acid mixture into distinct radioactive peaks with molecular weights in the 80-90 kD, 53-66 kD, 22-46 kD, and 17 kD ranges with isoelectric points between 5.0 and 7.9. Most of the amino acids were incorporated into proteins in all of the molecular weight ranges. But Ser was incorporated in highest amounts in the 17 kD range, and Val was most abundant in the 22-46 kD range. In some cases results indicated that single proteins were modified by several amino acids. While we do not yet know which amino acids modify specific nerve proteins or the function of the modifications in nerve regeneration, these studies demonstrate the participation of some but not all amino acids in posttranslational modification reactions and the selective modification of specific groups of nerve proteins by these amino acids.

Amino Acids↗