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Biomedical subjects

J L Ensunsa

Publications and source records attributed to J L Ensunsa.

8 recordsLinked to original sources
PubMed2001

Chocolate procyanidins decrease the leukotriene-prostacyclin ratio in humans and human aortic endothelial cells.

BACKGROUND: Polyphenolic phytochemicals inhibit vascular and inflammatory processes that contribute to disease. These effects are hypothesized to result from polyphenol-mediated alterations in cellular eicosanoid synthesis. OBJECTIVE: The objective was to determine and compare the ability of cocoa procyanidins to alter eicosanoid synthesis in human subjects and cultured human aortic endothelial cells. DESIGN: After an overnight fast, 10 healthy subjects (4 men and 6 women) consumed 37 g low-procyanidin (0.09 mg/g) and high-procyanidin (4.0 mg/g) chocolate; the treatments were separated by 1 wk. The investigation had a randomized, blinded, crossover design. Plasma samples were collected before treatment and 2 and 6 h after treatment. Eicosanoids were quantitated by enzyme immunoassay. Endothelial cells were treated in vitro with procyanidins to determine whether the effects of procyanidin in vivo were associated with procyanidin-induced alterations in endothelial cell eicosanoid synthesis. RESULTS: Relative to the effects of the low-procyanidin chocolate, high-procyanidin chocolate induced increases in plasma prostacyclin (32%; P<0.05) and decreases in plasma leukotrienes (29%; P<0.04). After the in vitro procyanidin treatments, aortic endothelial cells synthesized twice as much 6-keto-prostaglandin F(1alpha) (P<0.01) and 16% less leukotriene (P<0.05) as did control cells. The in vitro and in vivo effects of procyanidins on plasma leukotriene-prostacyclin ratios in culture medium were also comparable: decreases of 58% and 52%, respectively. CONCLUSION: Data from this short-term investigation support the concept that certain food-derived flavonoids can favorably alter eicosanoid synthesis in humans, providing a plausible hypothesis for a mechanism by which they can decrease platelet activation in humans.

Adult↗
PubMed2000

A dose-response effect from chocolate consumption on plasma epicatechin and oxidative damage.

Evidence from epidemiological studies suggests that a diet high in plant foods and rich in polyphenols is inversely associated with a risk for cardiovascular and other chronic diseases. Chocolate, like red wine and green tea, is a polyphenol-rich food, primarily containing procyanidin polyphenols. These polyphenols are hypothesized to provide cardioprotective effects due to their ability to scavenge free radicals and inhibit lipid oxidation. Herein, we demonstrate that 2 h after the ingestion of a procyanidin-rich chocolate containing 5.3 mg total procyanidin/g, of which 1.3 mg/g was (-)-epicatechin (epicatechin), plasma levels of epicatechin increased 133 +/- 27, 258 +/- 29 and 355 +/- 49 nmol/L in individuals who consumed 27, 53 and 80 g of chocolate, respectively. That the rise in plasma epicatechin levels was functionally significant is suggested by observations of trends for dose-response increases in the plasma antioxidant capacity and decreases in plasma lipid oxidation products. The above data support the theories that in healthy adults, 1) a positive relationship exists between procyanidin consumption and plasma procyanidin concentration and 2) the rise in plasma epicatechin contributes to the ability of plasma to scavenge free radicals and to inhibit lipid peroxidation.

Adult↗
PubMed1998

The influence of manganese deficiency on serum IGF-1 and IGF binding proteins in the male rat.

Young male rats subjected to a dietary manganese (Mn) deficiency respond to the deficiency by reducing their growth rate. The growth hormone (GH)/insulin-like growth factor (IGF) axis is critical for linear growth; this system is exquisitely sensitive to the nutritional state of the animal. In this study, we examined circulating GH, IGF-1, and insulin levels in Mn-deficient (-Mn; fed a 0.5 microg Mn/g diet) and sufficient (+Mn; fed a 45 microg Mn/g diet) male Sprague-Dawley rats. Additionally, we examined the distribution of circulating IGF binding proteins (IGFBPs) in animals of both dietary groups as these proteins modulate IGF-1 action in vivo and in vitro, and have been demonstrated to be altered in a number of nutritional and physiological states. Body weight was significantly reduced in -Mn relative to +Mn rats. Consistent with other studies, daily food intake was not altered. However, cumulative food intake (over 3 months) was marginally lower in -Mn versus +Mn animals. -Mn animals displayed lower circulating concentrations of IGF-1 (66% of control levels) and insulin (60% of control levels) despite having significant elevations in circulating GH levels relative to +Mn animals (140% of control levels). The IGFBP profile of -Mn animals reflected their elevated GH status, as we observed increased binding of tracer (125I-IGF-1) to the circulating IGFBP-3 complex (120% of control binding) using native chromatography techniques. Interestingly, the lower circulating insulin concentrations of -Mn animals did not result in dramatic elevations in lower-molecular-weight binding proteins. In summary, we demonstrate that in young male rats, Mn deficiency is associated with alterations in IGF metabolism. These alterations may contribute to the growth and bone abnormalities observed in -Mn animals.

Animals↗
PubMed1993

Catabolism of cysteine, cystine, cysteinesulfinate, and OTC by isolated perfused rat hindquarter.

The metabolism of cysteine and related compounds was investigated in the isolated perfused hindquarter of the rat. An erythrocyte-based perfusion medium was used; use of a perfluorochemical emulsion, FC-43, resulted in apparent chemical oxidation of cysteine, whereas bovine erythrocytes did not appear to contribute significantly to the metabolism of cysteine. Rat skeletal muscle perfused with L-[35S]cysteine, L-[35S]cystine, L-[35S]cysteinesulfinate, or L-2-oxo-[35S]thiazolidine-4-carboxylate (OTC) for 2 h produced [35S]sulfate and [35S]taurine. In all cases, the partitioning of cysteine or cysteinesulfinate between metabolism to taurine and sulfate was similar, suggesting that cysteine metabolism in hindquarter may occur via formation and catabolism of cysteinesulfinate by either cysteinesulfinate decarboxylase or aspartate (cysteine-sulfinate) aminotransferase. However, the activity of cysteine dioxygenase was extremely low, suggesting that the conversion of cysteine to cysteinesulfinate may have been non-enzymatic.

Adenine Nucleotides↗
PubMed1988

Albumin improves stability and longevity of perfluorochemical-perfused hearts.

We determined the effect of protein and nonprotein oncotic agents on physiological function and substructural integrity of perfluorochemical emulsion-perfused isolated working rabbit hearts. We used four media that contained Fluosol-43 (FL) emulsion and either 3.4% hydroxyethylstarch (HES), 2.9% albumin, 0.8% HES, or neither HES nor albumin (n = 5 hearts/group). All four groups of hearts had stable function for the first 5.5 h of perfusion; the FL plus albumin hearts continued to exhibit stability in most indexes of function until 9.5 h. The FL plus albumin hearts had a longer total period of ejecting function (12.5 +/- 0.5 h) compared with the other groups (mean longevities = 7.4-8.4 h). Functional stability and longevity correlated with maintenance of coronary flow and coronary vascular resistance. The rates of excess fluid accumulation and creatine kinase leakage were lower in the FL plus albumin hearts than in the other groups. We conclude that: 1) albumin maintained function, coronary flow, and myocardial cell integrity of FL-perfused hearts better than did HES; 2) albumin may exert its effect by preserving capillary permeability, thereby reducing the rate of interstitial fluid accumulation and preventing edema-induced vascular compression; and 3) HES had no effect on cardiac function or integrity and was ineffective in preventing interstitial fluid accumulation when it was used in FL-perfused isolated hearts in the absence of protein.

Animals↗
PubMed1987

Prolonged support of working rabbit hearts using Fluosol-43 or erythrocyte media.

We compared the perfluorochemical emulsion Fluosol-43 and an erythrocyte-based solution as support media for ex vivo working rabbit hearts functioning with a physiological workload. Both groups of hearts (n = 5/group) exhibited stable function (left ventricular peak systolic pressure, peak rates of left ventricular pressure rise and relaxation, aortic flow, peak aortic flow rate, stroke work, and peak power) for the first 6 h of perfusion. Coronary flow, coronary venous O2 content, and O2 supply-to-demand ratio declined similarly in both groups during the first 6 h. Both groups of hearts preferentially utilized pyruvate to glucose. The Fluosol-43-perfused hearts had higher heart rate, left ventricular peak systolic pressure, peak rate of left ventricular pressure rise, aortic flow, coronary flow, and myocardial O2 consumption compared with the erythrocyte-perfused hearts. The Fluosol-43 hearts produced more lactate and released more creatine phosphokinase than did the erythrocyte-perfused hearts, but the rates were low and constant throughout perfusion, indicating that the hearts were not progressively ischemic. After the first 6 h, function of the Fluosol-43 hearts declined, resulting in their earlier failure compared with the erythrocyte-perfused hearts. The data indicate that Fluosol-43 had sufficient O2- carrying capacity to support stable function of a rabbit heart at a physiological workload for 6 h, and differences in function and ex vivo longevity of the two groups of hearts suggested that a component or contaminant of Fluosol-43 altered sarcolemmal function and/or that a component needed for membrane integrity was lacking in the Fluosol-43 perfusate.

Animals↗
PubMedDate not supplied

Nutritional aspects of manganese from experimental studies.

In experimental animals, dietary manganese deficiency can result in numerous biochemical and structural abnormalities. Deficient animals can be characterized by impaired insulin production, alterations in lipoprotein metabolism, an impaired oxidant defense system, and perturbations in growth factor metabolism. If the deficiency occurs during early development, there can be pronounced skeletal abnormalities and an irreversible ataxia. Several lines of evidence suggest that manganese deficiency may be a problem in some human populations. Manganese toxicity can also pose a significant health risk. In experimental animals, acute manganese toxicity can result in numerous biochemical pathologies. However, the above occurs typically when the manganese is given via injection; most animals show considerable resistance to dietary manganese toxicosis. Similarly, confirmed cases of manganese toxicity in humans are currently restricted to cases of exposure to high levels of airborne manganese, and to cases when manganese excretory pathways are compromised.

Animal Nutritional Physiological Phenomena↗