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R M Russell

Publications and source records attributed to R M Russell.

At least 73 records · Page 4Linked to original sources

Effect of vitamin E supplementation on prostaglandin concentrations in aspirin-induced acute gastric injury in aged rats.

Nonsteroidal antiinflammatory drugs (NSAIDs), such as aspirin, frequently cause gastric mucosal injury in the elderly. Impairment of prostaglandin synthesis is a crucial step by which aspirin attenuates mucosal defense capacity. Vitamin E has been shown to decrease prostanoid concentrations, which implies an ulceropermissive effect of vitamin E. To assess the effect of vitamin E on aspirin-induced gastric injury and mucosal prostanoid concentrations, 20 male rats aged 20 mo were divided into two groups and fed diets containing either 30 (physiologic requirement) or 500 mg all-rac-alpha-tocopheryl acetate/kg. After 6 wk, all rats received two intragastric doses of aspirin (1.4 mumol/kg body wt). A third group of six animals fed the high-vitamin E diet received a vehicle solution without aspirin. Mucosal samples for vitamin E and prostaglandin E2, 6-keto-prostaglandin F1 alpha, and thromboxane A2 measurements were collected. The prevalence and degree of mucosal lesions were not significantly different among all groups. Rats fed the high-vitamin E diet had significantly higher mucosal vitamin E concentrations than rats fed the low-vitamin E diet. Mucosal concentrations of all three prostanoids were 95% lower in aspirin-treated rats than in controls (P = 0.0001 in all instances). The high-vitamin E diet group had significantly lower mucosal 6-keto-prostaglandin F1 alpha concentrations (P = 0.02) than the low-vitamin E diet group, indicating decreased prostacyclin formation, whereas concentrations of prostaglandin E2 and thromboxane A2 were similar in the aspirin-treated groups. Aspirin markedly reduced mucosal prostanoid concentrations in rats, without apparent effects on gastric injury, whereas vitamin E supplementation significantly reduced mucosal 6-keto-prostaglandin F(1 alpha) concentrations. Nevertheless, vitamin E supplementation did not result in more gastric injury in aspirin-treated rats than in controls.

6-Ketoprostaglandin F1 alpha↗

Beta-carotene isomers in human serum, breast milk and buccal mucosa cells after continuous oral doses of all-trans and 9-cis beta-carotene.

The concentrations of all-trans beta-carotene (tBC) and 9-cis beta-carotene (9cBC) isomers in serum, breast milk and buccal mucosa cells were determined after continuous oral doses as a simple, non-invasive method to determine whether differences in tissue uptake are important determinants of serum responses. Twelve healthy lactating women were recruited for a nonresidential study. On d 1, blood samples were obtained from fasting subjects for baseline concentrations of beta-carotene isomers. Over a 1-wk period, subjects were given either seven doses of a placebo (n = 4) or seven doses of naturally occurring BC (n = 8) derived from Dunaliella bardawil (64 mg tBC, 69 mg 9cBC). Subjects were instructed to consume a single beta-carotene dose along with a meal containing adequate fat each day for 1 wk. On d 2, 3, 5 and 8, blood samples and breast milk were collected from fasting subjects. On d 1 and 8, buccal mucosa cells were collected. Samples were analyzed for carotenoids by HPLC. In the experimental group, the mean serum concentration of tBC significantly increased to seven times the baseline level by the end of the supplementation period (P < 0.0001). The serum concentration of 9cBC significantly increased to three times the baseline level by the end of the supplementation period (P < 0.0001). The changes in milk and buccal mucosa cells levels of tBC and 9cBC followed a pattern similar to that for serum, showing significant increases at the end of the supplementation period. In the control group, the serum, milk and buccal mucosa cell concentrations of BC isomers did not change. This study confirms the previously reported differences in the serum response curves of tBC and 9cBC and provides evidence that there is no difference in tissue uptake of tBC and 9cBC.

Administration, Oral↗

Total intestinal lactase and sucrase activities are reduced in aged rats.

Lactase-phlorizin hydrolase (LPH) and sucrase-isomaltase (SI) are intestinal microvillus membrane hydrolases that play important roles in carbohydrate digestion. Although the expression of these enzymes during postnatal development has been characterized, the effect of old age on disaccharidase activity is poorly understood. In the present investigation, we examined the effect of aging on lactase and sucrase activities and their mRNA levels in the small intestines of 3-, 12- and 24- mo-old rats by sampling from nine equidistant segments of small intestine. Total intestinal disaccharidase activity or mRNA abundance was determined from areas under the proximal-to-distal curves. Rats 24 mo of age had total intestinal lactase and sucrase activities that were 12 and 38% lower, respectively, than the 3-mo-old animals (P < 0.05). In contrast, total LPH and SI mRNA abundance did not change significantly. Thus, total intestinal lactase and sucrase activities decrease with age in a manner that likely involves a posttranscriptional process. The age-related decline in disaccharidase activity, if extrapolated to humans, may have important implications for the digestion of carbohydrate contained in the diet of the elderly.

Aging↗

Ingestion by men of a combined dose of beta-carotene and lycopene does not affect the absorption of beta-carotene but improves that of lycopene.

A double-blind study was conducted in 10 healthy men to investigate serum beta-carotene and lycopene responses after ingestion of individual and combined doses of beta-carotene (BC) and lycopene. On each dosing day, a baseline blood sample was drawn, followed by an oral dose of 0.11 mmol (60 mg) of either all-trans BC or all-trans lycopene or by a combined oral dose of 0.11 mmol each. Subjects were tested with each of the three doses. The dose type was randomized. Blood (10 mL) was drawn at 1, 3, 5, 7, 9, 12 and 24 h after dosing. At 2 and 4 wk after the first dose, the protocol was repeated with the other doses. After ingestion of the BC dose, serum BC concentrations significantly decreased from baseline at 1 and 3 h followed by a continuous increase from baseline that was significant at 12 and 24 h (P < 0.01). Serum lycopene concentrations significantly increased from baseline at 5 h after the lycopene dose (P < 0.008) and returned to baseline thereafter. Ingestion of a combined dose of BC and lycopene resulted in a significant increase in serum concentrations of both BC and lycopene at 24 h (P < 0.05). The 24-h area under the curve (AUC) for BC was not different when BC was ingested alone or with lycopene, whereas the 24-h AUC for lycopene was significantly greater when lycopene was ingested with BC than when ingested alone (P < 0.05). Our data suggest that ingestion of a combined dose of BC and lycopene has little effect on the absorption of BC but improves that of lycopene in men.

Administration, Oral↗

Experimentally induced upper facial third fractures in unembalmed human cadaver heads.

Considerable need exists in the transportation industry to develop safety guidelines to protect the head and neck. One of the goals of this study was to produce facial fractures similar to those induced in motor vehicle crashes. Unembalmed cadaver heads were fixed to a supporting device and impacted with a steel pipe. The most common fracture was of the frontal sinus; multiple orbital wall, naso-orbitoethmoid, Le Fort I, II, and III fractures were also produced. Average impact speeds of 7.2 meters per second striking at the supraorbital rims created severe injury to both skull and contents. Energy absorption values accounted for the actual total contact time between head and pipe with tolerance level values measuring the force at specific intervals. The method described may be used to reproduce reliably those forces resulting in the facial fractures seen in the emergency room setting after motor vehicle crashes.

Acceleration↗

The impact of disease states as a modifying factor for nutrition toxicity.

Acquired kidney and liver diseases are relatively common diseases that can raise the potential for nutrient intoxication. For example, high-protein diets increase glomerular blood flow and the blood pressure gradient across the glomerular capillary wall in the kidney, which can result in injury to membranes. Likewise, the liver can increase nutrient intoxication because it is involved in the intermediary metabolism of many nutrients, serves as the storage organ for many nutrients, and is important in the biotransformation and excretion of nutrients. In this paper, vitamin A serves as an example to illustrate how kidney disease and liver disease can increase a single nutrient's toxicity.

Anemia, Pernicious↗

Dietary modification of human macular pigment density.

PURPOSE: The retinal carotenoids lutein (L) and zeaxanthin (Z) that form the macular pigment (MP) may help to prevent neovascular age-related macular degeneration. The purpose of this study was to determine whether MP density in the retina could be raised by increasing dietary intake of L and Z from foods. METHODS: Macular pigment was measured psychophysically for 13 subjects. Serum concentrations of L, Z, and beta-carotene were measured by high-performance liquid chromatography. Eleven subjects modified their usual daily diets by adding 60 g of spinach (10.8 mg L, 0.3 mg Z, 5 mg beta-carotene) and ten also added 150 g of corn (0.3 mg Z, 0.4 mg L); two other subjects were given only corn. Dietary modification lasted up to 15 weeks. RESULTS: For the subjects fed spinach or spinach and corn, three types of responses to dietary modification were identified: Eight "retinal responders" had increases in serum L (mean, 33%; SD, 22%) and in MP density (mean, 19%; SD, 11%); two "retinal nonresponders" showed substantial increases in serum L (mean, 31%) but not in MP density (mean, -11%); one "serum and retinal nonresponder" showed no changes in serum L, Z, or beta-carotene and no change in MP density. For the two subjects given only corn, serum L changed little (+11%, -6%), but in one subject serum Z increased (70%) and MP density increased (25%). CONCLUSIONS: Increases in MP density were obtained within 4 weeks of dietary modification for most, but not all, subjects. When MP density increased with dietary modification, it remained elevated for at least several months after resuming an unmodified diet. Augmentation of MP for both experimental and clinical investigation appears to be feasible for many persons.

Adult↗

Beta-oxidation in rabbit liver in vitro and in the perfused ferret liver contributes to retinoic acid biosynthesis from beta-apocarotenoic acids.

The biosynthesis of retinoic acid from beta-apocarotenoic acids was examined for a beta-oxidation-like process using both rabbit liver mitochondrial fractions with various beta-apocarotenoic acids (beta-apo-14'-, beta-apo-12'-, and beta-apo-8'-carotenoic acid) and perfusion in ferret liver through the portal vein with beta-apo-8'-carotenoic acid. The in vitro incubation of beta-apo-8', beta-apo-12'-, and beta-apo-14'-carotenoic acids gave rise to shorter chain beta-apocarotenoic acids as well as retinoic acid. The rate of retinoic acid synthesis from 10 microM beta-apo-8', beta-apo-12'-, and beta-apo-14'-carotenoic acids was 11 +/- 2, 18 +/- 3, and 30 +/- 7 pmol/h/mg of protein, respectively. The stepwise oxidation of beta-apocarotenoic acid in mitochondria was dose-related to both protein concentration and substrate concentration. beta-Apocarotenoic acid oxidation was inhibited in a dose-dependent manner when it was co-incubated with oleoyl-CoA. The in vivo perfusion of ferret liver with beta-apo-8'-carotenoic acid resulted in a linear increase in the retinoic acid concentration of bile, which was completely abolished by co-perfusion of 3-mercaptopropionic acid, an inhibitor of long chain acyl-CoA dehydrogenase, and partially inhibited by 2-tetradecylglycidic acid, an inhibitor of carnitine-palmitoyl-CoA transferase I. However, the formation of retinoic acid from the beta-apocarotenoic acids was not inhibited, either in vitro or in vivo, by citral, an inhibitor of retinal oxidase. Thus, the formation of retinoic acid was not occurring by the central cleavage pathway. These data suggest that the oxidation of intermediate compounds between beta-carotene and retinoic acid may undergo a type of beta-oxidative process to form retinoic acid, which is reminiscent of mitochondrial fatty acid beta-oxidation. This pathway may play an important role in the biosynthesis of retinoic acid from beta-carotene.

Animals↗

Carotenoids, vitamins C and E, and mortality in an elderly population.

In 1981-1984, the nutritional status of 747 noninstitutionalized Massachusetts residents aged 60 years and over was assessed. Nine to 12 years later, the vital status of these subjects was determined. The data of a subset of 725 community-dwelling volunteers was used to examine associations between mortality and the nutrient antioxidants (carotenoids and vitamins C and E) in plasma, diet, and supplements. Results indicated that subjects with plasma vitamin C levels in the middle and high quintiles had a lower overall mortality (relative risk (RR) = 0.64, 95% confidence interval (CI) 0.44-0.94 and RR = 0.54, 95% CI 0.32-0.90, respectively) than those in the lowest quintile even after adjustment for potential confounders. These associations were largely due to reduced mortality from heart disease. Subjects in the highest quintile of total intake of vitamin C also had a significantly lower risk of overall mortality (RR = 0.55, 95% CI 0.32-0.93) and mortality from heart disease (RR = 0.38, 95% CI 0.19-0.75) than did those in the lowest quintile after potential confounders were controlled for. Intake of vegetables was inversely associated with overall mortality (p for trend = 0.003) and mortality from heart disease (p for trend = 0.04). No other significant associations were observed. In conclusion, the results indicate that high intakes and plasma levels of vitamin C and frequent consumption of vegetables may be protective against early mortality and mortality from heart disease.

Age Distribution↗

Nutrition.

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Coronary Disease↗

Use of albumin as a predictor of mortality in community dwelling and institutionalized elderly populations.

This study was undertaken to identify variables that could explain the association between low albumin and a 9- to 12-year mortality follow-up among 287 community- dwelling and 176 institutionalized people aged 60 years and over. A wide array of nutrition assessment variables was simultaneously examined in this population to identify confounders of the association. The results show that the risk of mortality for subjects with albumin values of 40 g/liter and over was 0.46 of the risk for those with albumin values below 40 g/liter, after controlling for the confounders age, blood urea nitrogen, triglyceride, history of diseases, and inability to shop owing to medical conditions. Similarly, albumin was also inversely associated with mortality among institutionalized subjects even after controlling for the confounders age, sex, blood urea nitrogen, transferrin, and history of stroke. However, the association was no longer significant among the institutionalized population once the deaths that occurred within the first 3 years after study participation were eliminated. The results indicate that albumin is a long-term predictor of mortality among noninstitutionalized subjects and increased mortality is not only a result of age, history of chronic diseases, medication use, or protein intake. Among institutionalized subjects, albumin appeared to be a short-term predictor of mortality.

Aged↗

Serum response of all-trans and 9-cis isomers of beta-carotene in humans.

OBJECTIVE: Little work has been performed on the serum response of various carotene isomers. The present study was carried out to examine the serum response of all-trans and 9-cis isomers of beta-carotene (BC) using frequent blood sample collections at early time points. METHODS: Serum responses of all-trans BC and a mixture of BC isomers containing 80% 9-cis BC were studied in 15 men by measuring the serum concentrations of BC at 1, 3, 5, 7, 9, 12, and 24 hours after a single large oral dose of all-trans BC or 9-cis BC. RESULTS: The serum response to an oral dose of all-trans BC (120 mg) significantly increased from baseline at 24 hr (p < 0.004). After an oral dose of a mixture of BC isomers (120 mg, 80% 9-cis BC), the peak concentration of 9-cis BC was significantly greater that baseline values (p < 0.016). CONCLUSIONS: Increases in serum all-trans BC levels, in part, may be due to greater intestinal absorption, whereas the inability to measure a significant increase in the concentration of 9-cis BC may indicate poor absorption, isomerization to all-trans BC, or a very rapid tissue uptake.

Adult↗

Human plasma carotenoid response to the ingestion of controlled diets high in fruits and vegetables.

Plasma carotenoid responses were determined in 36 healthy men and women before and after being fed controlled diets with a moderate amount of fat (26% of total energy) and a high carotenoid content (approximately 16 mg/d) for two 15-d periods. In addition, broccoli (205 g/d) was provided either during the first or the second 15-d residency period in a crossover design. Plasma was digested with lipase and cholesterol esterase, and carotenoids were extracted and measured by using HPLC. Three oxygenated carotenoids (lutein, zeaxanthin, and cryptoxanthin), three hydro-carbon carotenoids (alpha-carotene, all-trans-beta-carotene, and 13-cis-beta-carotene), and four geometric isomers of lycopene (15-cis-, 13-cis-, 9-cis-, and all-trans-lycopene) were separated by using a C30 carotenoid column. A small unidentified peak coeluted with standard 9-cis-beta-carotene and was identified as zeta-carotene (lambda(max) = 400 nm). The concentrations of plasma lutein, cryptoxanthin, alpha-carotene, 13-cis-beta-carotene, all-trans-beta-carotene, and cis- and trans-lycopenes were all significantly increased (P < 0.05) on days 6-16 by the high-fruit and -vegetable diets. The provision of additional broccoli for 5 d to the basic high-carotenoid diet resulted in a further significant increase in the serum concentration of lutein compared with the feeding of the basic high-carotenoid diet alone. Most of the measurable carotenoids of human plasma can be increased by moderate alterations in diet within a short time, although the magnitude of the plasma response may be related to the baseline carotenoid concentrations.

Adult↗

Gastric acidity influences the blood response to a beta-carotene dose in humans.

The effect of gastric acidity on the blood response to a single dose of 120 mg beta-carotene in humans was investigated in 12 normal subjects (5 women, 7 men) aged 23-68 y. Omeprazole was used for 7 d to obliterate gastric acid secretion and to raise gastric pH to > 4.5. In a crossover design, six subjects were randomly assigned to take beta-carotene with omeprazole either at the beginning (day 9) or at the end (day 26) of the study. The beta-carotene response in blood was not altered by the experimental order. Results from the high-gastric-pH phase (ie, with omeprazole) were analyzed together and compared with the results from the low-gastric-pH phase (ie, without omeprazole). The increases of serum concentrations of both trans beta-carotene and cis beta-carotene 6 and 24 h after the beta-carotene dose were significantly greater at a low gastric pH (pH = 1.3 +/- 0.1, ie, without omeprazole) than those at a high gastric pH (pH = 6.4 +/- 0.3, ie, with omeprazole), P < 0.02. Similarly, 24 h after beta-carotene administration, the area under the blood beta-carotene response curve (trans plus cis beta-carotene) was significantly greater at a low gastric pH (6825 +/- 760 nmol.h/L) than at a high gastric pH (3390 +/- 550 nmol.h/L), P < 0.002. In investigations of bacterial overgrowth, gelatin capsule disintegration and isomeric profiles associated with high and low pH, we could not identify factors to explain the differences observed in the blood response curves between low-gastric-pH and high-gastric-pH conditions. A suppressed blood response of beta-carotene at a high intraluminal pH may have been due to the slower movement of negatively charged micelles through the unstirred water layer and cell membrane.

Absorption↗

Gastric emptying and first-pass metabolism of ethanol in elderly subjects with and without atrophic gastritis.

BACKGROUND: Oral ethanol intake results in lower blood ethanol concentrations than intravenous administration of the same dose of ethanol. This first-pass metabolism is thought to be due to gastric metabolism of ethanol via alcohol dehydrogenase and also to hepatic first-pass metabolism. METHODS: Since a loss of gastric mucosa may decrease first-pass metabolism of ethanol, this metabolism was studied in 10 elderly subjects (6 women and 4 men) with atrophic gastritis and bacterial overgrowth and in 17 control subjects with normal gastric secretory function. Atrophic gastritis was verified by means of the serum pepsinogen I to pepsinogen II ratio and the hypochlorhydria occurring after pentagastrin stimulation. Bacterial overgrowth was assessed by bacteria. In addition, gastric emptying rates of ethanol solution with technetium-99m sulfur colloid were calculated from scintigraphic images. Furthermore, gastric biopsy specimens were taken from 12 female patients with atrophic gastritis and from 12 controls for determination of alcohol dehydrogenase activity. RESULTS: Neither gender (female versus male, 28 +/- 5% versus 42 +/- 5%), atrophic gastritis (normal versus atrophic gastritis, 35 +/- 4% versus 32 +/- 6%), nor tetracycline treatment in atrophic gastritis subjects (before versus after, 32 +/- 6% versus 41 +/- 5%) had a statistically significant effect on the first-pass metabolism of ethanol in the elderly. Gastric alcohol dehydrogenase activity was significantly lower in atrophic gastritis subjects than in controls (p < 0.01). A significant correlation was found between the first-pass metabolism of ethanol in healthy controls and gastric half-emptying time (p = 0.032). CONCLUSIONS: We conclude from these data that the rate of gastric emptying modulates first-pass metabolism of ethanol in elderly individuals.

Aged↗