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Biomedical subjects

M A Leo

Publications and source records attributed to M A Leo.

At least 19 recordsLinked to original sources
PubMed2001

Alcohol and retinoids.

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Hirokazu Yokoyama and David Crabb. The presentations were (1) Roles of vitamin A, retinoic acid, and retinoid receptors in the expression of liver ALDH2, by J. Pinaire, R. Hasanadka, M. Fang, and David W. Crabb; (2) Alcohol, vitamin A, and beta-carotene: Adverse interactions, by M. A. Leo and Charles S. Lieber; (3) Retinoic acid, hepatic stellate cells, and Kupffer cells, by Hidekazu Tsukamoto, K. Motomura, T. Miyahara, and M. Ohata; (4) Retinoid storage and metabolism in liver, by William Bosron, S. Sanghani, and N. Kedishvili; (5) Characterization of oxidation pathway from retinol to retinoic acid in esophageal mucosa, by Haruko Shiraishi, Hirokazu Yokoyama, Michiko Miyagi, and Hiromasa Ishii; and (6) Ethanol in an inhibitor of the cytosolic oxidation of retinol in the liver and the large intestine of rats as well as in the human colon mucosa, by Ina Bergheim, Ina Menzl, Alexandr Parlesak, and Christiane Bode.

Aldehyde Dehydrogenase↗
PubMed2001

Effect of beta-carotene on hepatic cytochrome P-450 in ethanol-fed rats.

BACKGROUND: Hepatotoxicity of ethanol is increased by beta-carotene in both rodents and nonhuman primates. Furthermore, in smokers who are also drinkers, beta-carotene increases the incidence of pulmonary cancer. The hepatotoxicity was associated with proliferation of the membranes of the smooth endoplasmic reticulum, suggesting the involvement of cytochromes P-450. Therefore, the aim of the present study was to assess the effect of beta-carotene and ethanol treatment on rodent hepatic cytochromes P-450. METHODS AND RESULTS: Weanling male Sprague-Dawley rats were pair-fed beta-carotene (56.5 mg/l of diet) for 8 weeks, with and without ethanol (Lieber-DeCarli, 1994 liquid diet). As expected, ethanol increased CYP2E1 (measured by Western blots) from 67 +/- 8 to 317 +/- 27 densitometric units (p < 0.001). Furthermore, beta-carotene potentiated the ethanol induction to 442 +/- 38 densitometric units (p < 0.01) with a significant interaction (p = 0.012). The rise was confirmed by a corresponding increase in the hydroxylation of p-nitrophenol, a specific substrate for CYP2E1, and by the inhibition with diethyl dithiocarbamate (50 microM). Beta-carotene alone also significantly induced CYP4A1 protein (328 +/- 49 vs. 158 +/- 17 densitometric units, p < 0.05). The corresponding CYP4A1 mRNA (measured by Northern blots) was also increased (p < 0.05) and there was a significant interaction of the two treatments (p = 0.015). The combination of ethanol and beta-carotene had no significant effect on either total cytochrome P-450 or CYP1A1/2, CYP2B, CYP3A, and CYP4A2/3 contents. CONCLUSIONS: Beta-carotene potentiates the CYP2E1 induction by ethanol in rat liver and also increases CYP4A1, which may, at least in part, explain the associated hepatotoxicity.

Animals↗
PubMed2000

Polyenylphosphatidylcholine protects against alcohol but not iron-induced oxidative stress in the liver.

BACKGROUND: We reported before that, in baboons, the alcohol-induced oxidative stress in the liver is associated with depletion of dilinoleoylphosphatidylcholine [the major component of polyenylphosphatidylcholine (PPC)] and that both can be corrected by the administration of PPC, but we did not determine whether this protection extended to iron-induced oxidative stress. METHODS: To compare the effects of PPC on alcohol- and iron-induced hepatic oxidative stress, 56 Sprague Dawley male rats were pair-fed nutritionally adequate liquid diets containing ethanol (36% of energy) or isocaloric carbohydrate and PPC (3 mg/ml) or safflower oil (2.73 mg/ml), with or without 5 mg/ml carbonyl iron for 2 months. Markers of oxidative stress (4-hydroxynonenal and reduced glutathione), antioxidants (vitamin E, ubiquinol-9, and ubiquinol-10), and phosphatidylcholine (PC) species were assessed by HPLC and/or gas chromatography/mass spectrometry. RESULTS: Alcohol feeding increased hepatic 4-hydroxynonenal 3-fold and decreased glutathione by 19%, ubiquinol-10 by 53%, and PC species containing arachidonate (palmitoyl- and stearoylarachidonoylphosphatidylcholines by 24% and 21%, respectively) and total phospholipids by 14%. PPC feeding prevented the rise of 4-hydroxynonenal, restored glutathione, and increased the hepatic content of dilinoleoylphosphatidylcholine and of some other PC carrying polyunsaturated fatty acids. Administration of iron alone increased hepatic iron, doubled 4-hydroxynonenal and glutathione, whereas it decreased vitamin E, ubiquinol-9, total phospholipids, and several polyunsaturated PC. Alcohol given with iron further exacerbated the hepatic oxidative stress, as documented by the increase of 4-hydroxynonenal and the decrease in glutathione and ubiquinols-10. PPC did not prevent this oxidative stress, although it increased hepatic glutathione. Hepatic dilinoleoylphosphatidylcholine content was comparable with and without dietary iron. CONCLUSIONS: PPC prevents the alcohol-induced oxidative stress but only in the absence of iron overload.

Animals↗
PubMed1999

Alcohol-induced pancreatic oxidative stress: protection by phospholipid repletion.

Oxidative stress is considered to be a forerunner of pancreatitis. Since we had found polyenylphosphatidylcholine, a mixture of polyunsaturated phosphatidylcholines extracted from soybeans, to protect against hepatic oxidative stress, we now tested its effects on the pancreas. Sprague-Dawley rats were pair-fed for two months nutritionally adequate liquid diet containing ethanol (36% of energy) or isocaloric carbohydrate, with either polyenylphosphatidylcholine (3 g/1000 kcal) or safflower oil, with or without 5 g/1000 kcal carbonyl iron. Parameters of oxidative stress (F2-isoprostanes, 4-hydroxynonenal, reduced glutathione), ubiquinol-10, ubiquinol-9 and vitamin E, as well as phosphatidylcholine species, were assessed by GC/MS and/or HPLC. Alcohol feeding increased pancreatic 4-hydroxynonenal three-fold, F2-isoprostanes and ubiquinol-9 by more than 70%, whereas it decreased total phospholipids, several phosphatidylcholine species, ubiquinol-10 and glutathione, especially in iron fed rats. Polyenylphosphatidylcholine prevented the rise in 4-hydroxynonenal and F2-isoprostanes, the decrease in dilinoleoylphosphatidylcholine and oleoyllinoleoylphosphatidylcholine and opposed the alcohol-induced decrease of glutathione; alpha-tocopherol remained unchanged. Iron had no significant effect except for decreasing ubiquinol-10 in the pancreas and increasing aminotransferases in the plasma. Thus, the alcohol-induced oxidative stress in the pancreas was shown to be prevented by polyenylphosphatidylcholine which may act, in part, by correcting the depletion of several phosphatidylcholine species.

Alcoholism↗
PubMed1999

Alcohol, vitamin A, and beta-carotene: adverse interactions, including hepatotoxicity and carcinogenicity.

Isozymes of alcohol and other dehydrogenases convert ethanol and retinol to their corresponding aldehydes in vitro. In addition, new pathways of retinol metabolism have been described in hepatic microsomes that involve, in part, cytochrome P450s, which can also metabolize various drugs. In view of these overlapping metabolic pathways, it is not surprising that multiple interactions between retinol, ethanol, and other drugs occur. Accordingly, prolonged use of alcohol, drugs, or both, results not only in decreased dietary intake of retinoids and carotenoids, but also accelerates the breakdown of retinol through cross-induction of degradative enzymes. There is also competition between ethanol and retinoic acid precursors. Depletion ensues, with associated hepatic and extrahepatic pathology, including carcinogenesis and contribution to fetal defects. Correction of deficiency through vitamin A supplementation has been advocated. It is, however, complicated by the intrinsic hepatotoxicity of retinol, which is potentiated by concomitant alcohol consumption. By contrast, beta-carotene, a precursor of vitamin A, was considered innocuous until recently, when it was found to also interact with ethanol, which interferes with its conversion to retinol. Furthermore, the combination of beta-carotene with ethanol results in hepatotoxicity. Moreover, in smokers who also consume alcohol, beta-carotene supplementation promotes pulmonary cancer and, possibly, cardiovascular complications. Experimentally, beta-carotene toxicity was exacerbated when administered as part of beadlets. Thus ethanol, while promoting a deficiency of vitamin A also enhances its toxicity as well as that of beta-carotene. This narrowing of the therapeutic window for retinol and beta-carotene must be taken into account when formulating treatments aimed at correcting vitamin A deficiency, especially in drinking populations.

Animals↗
PubMed1999

Polyenylphosphatidylcholine opposes the increase of cytochrome P-4502E1 by ethanol and corrects its iron-induced decrease.

Dietary iron overload damages membrane phospholipids and decreases microsomal cytochromes P-450. We wondered whether this might also pertain to cytochrome P-4502E1 (2E1) and whether polyenylphosphatidylcholine (PPC), a 94-96% pure mixture of linoleate-rich polyunsaturated phosphatidylcholines that protects against alcohol-induced liver injury, also affects 2E1, either in the presence or absence of iron. Accordingly, rats were fed for 8 weeks our standard liquid diet containing ethanol (36% of energy) or isocaloric carbohydrates, with either PPC (3 g/1000 Cal) or equivalent amounts of linoleate (as safflower oil). 2E1 was assessed by Western blots and by two of its characteristic enzyme activities: the microsomal ethanol oxidizing system (MEOS), evaluated by the conversion of ethanol to acetaldehyde (determined by head space GC), and p-nitrophenolhydroxylase (PNP) activity, measured by HPLC with UV detection of 4-nitrocatechol. With ethanol (36% of energy) replacing carbohydrates, 2E1 content increased 10-fold, with a corresponding increase in PNP and MEOS activities, but when carbonyl iron (5 g/1000 Cal) was added, the induction was significantly reduced. This iron-induced decrease was corrected by PPC. PPC is rich in linoleate, but when the latter was given as triglycerides (safflower oil), there was no effect, whereas hepatic nonheme iron content was the same in both these groups. It also was found that in the absence of iron, the ethanol-mediated induction of 2E1 and its corresponding enzyme activities were significantly less with PPC (< 0.001) than with safflower oil. In addition, in alcohol-fed animals, PPC decreased the oxidative stress (as determined by F2-isoprostanes), which reflects yet another hepatoprotective effect of PPC.

Animals↗
PubMed1999

Oxidation of LDL in baboons is increased by alcohol and attenuated by polyenylphosphatidylcholine.

Alcohol taken in moderation may prevent atherosclerosis, whereas heavy drinking has the opposite effect, in part by promoting oxidation of low density lipoproteins (LDL), a pathogenetic factor in atherogenesis. We assess here: 1 ) whether similar alterations can be reproduced in baboons fed 50% of energy as ethanol (the average intake of alcoholics) for 7- 8 years, and 2 ) whether such alterations are affected by supplementation with polyenylphosphatidylcholine (PPC), a mixture of polyunsaturated phosphatidylcholines, shown to prevent alcoholic fatty liver, fibrosis, and cirrhosis. Ten animals were given the ethanol-containing diet and ten were pair-fed isocaloric control diets. In half of the pairs, the diets were supplemented with 2.8 g of polyenylphosphatidylcholine/1000 kcal. Alcohol feeding increased LDL-lipoperoxides and made LDL-proteins more negatively charged, changes that were attenuated or prevented by PPC. The oxidizability of LDL was determined in vitro by the formation of conjugated dienes after oxidation with copper. Alcohol shortened the lag time (which measures LDL antioxidant capacity); this effect was normalized by PPC supplementation. By contrast, PPC produced no changes in the controls. Thus polyenylphosphatidylcholine, by markedly attenuating the ethanol-induced increase in LDL oxidation, opposes one of the effects whereby alcohol promotes atherosclerosis.

Animals↗
PubMed1999

Dilinoleoylphosphatidylcholine is the active antioxidant of polyenylphosphatidylcholine.

BACKGROUND: Polyenylphosphatidylcholine, a mixture of polyunsaturated phospholipids, prevents the fibrosis induced by alcohol in baboons and by CCl4 in rats and opposes the associated oxidative stress. METHODS: To determine the responsible phosphatidylcholine species, a Morris hepatoma cell line (RH 7777) was incubated with 100 mumol/L arachidonate supplemented with 20 mumol/L dilinoleoylphosphatidylcholine or 20 mumol/L palmitoyllinoleoylphosphatidylcholine which comprise 42% and 24% of polyenylphosphatidylcholine, respectively or with equivalent amounts of polyenylphosphatidylcholine. Distearoylphosphatidylcholine, the saturated analog of dilinoleoylphosphatidylcholine, also was used for comparison. Two markers of lipid peroxidation (4-hydroxynonenal and F2-isoprostanes) were measured by GC/MS. RESULTS: Arachidonate caused 8- and 11-fold rises of cellular 4-hydroxynonenal and F2-isoprostanes, respectively; these increases were reduced more than 50% by polyenylphosphatidylcholine and dilinoleoylphosphatidylcholine. By contrast, palmitoyllinoleoylphosphatidylcholine and distearoylphosphatidylcholine had no significant effect. Lipid peroxidation was associated with a striking exacerbation of cell death, observed microscopically, and documented by a 2.5-fold decrease in cellular DNA and a 2- to 3-fold increase in lactic dehydrogenase leakage. Dilinoleoylphosphatidylcholine and polyenylphosphatidylcholine decreased the release of lactic dehydrogenase (47% and 67%, respectively); whereas, palmitoyllinoleoylphosphatidylcholine had no effect. CONCLUSIONS: An in vitro system of oxidative stress revealed that polyenylphosphatidylcholine is a potent antioxidant and that dilinoleoylphosphatidylcholine is mainly responsible for this protective effect; whereas, its saturated counterpart distearoylphosphatidylcholine is inactive.

Animals↗
PubMed1998

Metabolism of ethanol and some associated adverse effects on the liver and the stomach.

Current knowledge of alcohol oxidation and its effects on hepatic metabolism and its toxicity are summarized. This includes an evaluation of the relationship of the level of consumption to its interaction with nutrients (especially retinoids, carotenoids, and folate) and the development of various stages of liver disease. Ethanol metabolism in the stomach and its link to pathology and Helicobacter pylori is reviewed. Promising therapeutic approaches evolving from newly gained insight in the pathogenesis of medical complications of alcoholism are outlined. At present, the established approach for the prevention and treatment of alcoholism are outlined. At present, the established approach for the prevention and treatment of alcoholic liver injury is to control alcohol abuse, with the judicial application of selective antioxidant therapy, instituted at early stages, prior to the social or medical disintegration of the patient, and associated with antiinflammatory agents at the acute phase of alcoholic hepatitis. In addition, effective antifibrotic therapy may soon become available.

Alcohol Dehydrogenase↗
PubMed1998

Increased circulating products of lipid peroxidation in patients with alcoholic liver disease.

F2-isoprostanes (F2-IP) and 4-hydroxynonenal (4-HNE), peroxidation products of polyunsaturated fatty acids (PUFA), are considered the most reliable indicators of endogenous lipid peroxidation in vivo. To determine to what extent these are also altered in patients with alcoholic liver disease, plasma free and esterified F2-IP as well as 4-HNE were measured by GC/MS in 49 fasting subjects who underwent diagnostic percutaneous needle biopsies of the liver. Compared to patients with mild steatosis and no fibrosis, free F2-IP and 4-HNE were strikingly increased in individuals with alcoholic hepatitis. There was also a significant but lesser rise of 4-HNE in patients with perivenular fibrosis. An increase of F2-IP was also found in subjects with transition to, or complete, alcoholic cirrhosis, with a comparable trend for 4-HNE. By contrast, in patients who were drinking heavily up to 48 hr before admission, F2-IP were not abnormal, but they increased later (p < 0.005). Contrasting with plasma free F2-IP, esterified F2-IP were not significantly changed with fibrosis. Thus, whereas circulating esterified F2-IP were unchanged in patients with alcoholic liver disease, there was an increase in free F2-IP as well as 4-HNE during recovery from intoxication. The increase was not a result of accompanying hepatitis C but a function of the stage of alcoholic liver injury, possibly reflecting enhanced lipid peroxidation as well as interference with biliary excretion and/or hepatic esterification.

Aldehydes↗
PubMed1997

Polyenylphosphatidylcholine prevents carbon tetrachloride-induced lipid peroxidation while it attenuates liver fibrosis.

BACKGROUND/AIMS: Polyenylphosphatidylcholine protects against alcoholic cirrhosis in the baboon and carbon tetrachloride-induced cirrhosis in rats. This study addresses the possible mechanism of the protective effect of polyenylphosphatidylcholine. METHODS: For 8 weeks, rats were injected with either carbon tetrachloride in peanut oil or peanut oil alone (control), and pair-fed nutritionally adequate liquid diets with equivalent amounts of linoleic acid either as polyenylphosphatidylcholine or as safflower oil. Other rats were injected for 9 weeks with heterologous albumin and fed the same liquid diets. Lipid peroxidation was measured by F2-isoprostanes and 4-hydroxynonenal. RESULTS: Carbon tetrachloride-induced lipid peroxidation was strikingly attenuated with polyenylphosphatidylcholine supplementation. Levels of hepatic F2-isoprostanes and 4-hydroxynonenal paralleled liver fibrotic scores and collagen accumulation. Polyenylphosphatidylcholine also attenuated the fibrosis induced in rats with human albumin, but in this case, levels of hepatic 4-hydroxynonenal did not change, nor were they significantly affected by polyenylphos-phatidylcholine. Neither carbon tetrachloride injection nor polyenylphosphatidylcholine treatment changed the arachidonic acid content (a major precursor of F2-isoprostanes and 4-hydroxynonenal) in liver phospholipids, and hepatic vitamin E was not significantly altered. CONCLUSIONS: The hepatic protection of polyenylphosphatidylcholine against carbon tetrachloride appears to be due, at least in part, to an antioxidant effect, whereas the protection against heterologous albumin-induced fibrosis suggests that an additional mechanism, such as stimulation of collagenase activity, may also be responsible.

Analysis of Variance↗
PubMed1997

beta-Carotene beadlets potentiate hepatotoxicity of alcohol.

Administration of beta-carotene in beadlets to baboons potentiates alcohol-induced liver injury. To determine whether this also occurs in other species, and whether the beadlet carrier itself contributes to the toxicity, rats were given for 2 mo vitamin A (1.4 U/J), beta-carotene (4.8, 12.0, and 24.0 U/J, with or without beadlets), or corresponding amounts of beadlets without beta-carotene, in diets containing either carbohydrates or equivalent amounts of ethanol. Isoenergetic substitution of ethanol (36% of total energy) for carbohydrates reduced hepatic vitamin A by 80%, and such a depletion was also observed with beta-carotene as vitamin A precursor. By contrast, ethanol raised hepatic beta-carotene, which was further increased by beadlets. Thus, whereas alcohol promoted hepatic depletion of vitamin A, it had the opposite effect on beta-carotene. Ethanol seems to affect the homeostasis of beta-carotene. Furthermore, the ethanol-induced oxidative stress, assessed by an increase in hepatic 4-hydroxynonenal and F2-isoprostanes (measured by gas chromatography-mass spectrometry), was not improved despite a concomitant rise in hepatic antioxidants (beta-carotene and vitamin E). Moreover, beadlets resulted in proliferation of the smooth endoplasmic reticulum and in leakage of the mitochondrial glutamate dehydrogenase into the plasma, reflecting mitochondrial injury (both documented by electron microscopy). Thus, in rats given ethanol, beta-carotene is not an efficient vitamin A precursor. Its bioavailability was improved by beadlets, but the ethanol-induced oxidative stress was not attenuated and there was associated hepatotoxicity that now needs to be assessed in humans.

Animals↗
PubMed1997

Polyenylphosphatidylcholine decreases alcohol-induced oxidative stress in the baboon.

Diets supplemented with polyunsaturated fatty acids or triglycerides exacerbate alcohol-induced liver injury in rats, whereas, in baboons, polyenylphosphatidylcholine (PPC) protects against alcohol-induced fibrosis and cirrhosis. Because the aggravation in rats was attributed to enhanced lipid peroxidation, the present study was undertaken to assess parameters of oxidative stress in percutaneous liver biopsies of baboons fed alcohol, with or without PPC (2.8 g per 1000 calories). F2-isoprostanes and 4-hydroxynonenal, breakdown products of lipid peroxidation, were determined by gas chromatography/mass spectrometry, and alpha-tocopherol was measured by HPLC with electrochemical detection. Hepatic 4-hydroxynonenal was significantly increased in animals fed alcohol, but this was fully prevented by PPC. F2-isoprostanes were also significantly lower after PPC and ethanol than after ethanol alone, and the alcohol-induced glutathione decrease was attenuated. All of these parameters were normal in the animals withdrawn from alcohol, even with persistence of significant liver disease. Because peroxidation products are fibrogenic, their decrease could contribute to the antifibrogenic property of the phospholipids. In conclusion, PPC significantly attenuates ethanol-induced oxidative stress, which may explain, at least in part, its protective effect against alcoholic liver injury.

Alcoholism↗
PubMed1997

F2-isoprostane and 4-hydroxynonenal excretion in human bile of patients with biliary tract and pancreatic disorders.

OBJECTIVE: To assess parameters of lipid peroxidation in bile of patients with hepatobiliary and pancreatic diseases. METHODS: F2-isoprostanes (F2-IPs) and 4-hydroxynonenal (4-HNE) were measured in bile collected during 31 ERCP procedures using gas chromatography/mass spectrometry. RESULTS: In 11 subjects with normal ERCP (controls), bile contained significant amounts of F2-IPs (188 +/- 27 pg/ml) and 4-HNE (37.5 +/- 8.0 ng/ml). In 10 individuals with bile duct stones, there was a 3-fold increase of F2-IPs (523 +/- 129 pg/ml; p < 0.05) and a 2.5-fold increase of 4-HNE (89.6 +/- 18.0 ng/ml; p < 0.05). In 10 patients with various pancreatic diseases, bile F2-IPs were also enhanced (545 +/- 112 pg/ml; p < 0.01). There was no significant change in alpha-tocopherol, whereas beta-carotene was decreased in biliary tract and pancreatic diseases (p < 0.05). Results of serum liver tests were normal with the exception of bilirubin, which was increased together with alkaline phosphatase. Concentrations of total lipids, phospholipids, and cholesterol did not differ significantly between the three groups. CONCLUSIONS: These data provide the first evidence in humans supporting the role of oxidative stress in the pathogenesis of biliary and pancreatic disease.

Aged↗
PubMed1995

Carotenoids and tocopherols in various hepatobiliary conditions.

BACKGROUND: Previous studies revealed hepatic interactions of beta-carotene with alcohol in non-human primates, but bile carotenoids and alpha-tocopherol have not previously been explored in man. METHODS: To compare the plasma and biliary concentrations of carotenoids, retinoids and tocopherols among controls and patients with biliary and pancreatic diseases, these compounds were measured by high performance liquid chromatography in bile collected during 41 endoscopic retrograde cholangiopancreatographies. RESULTS: In 14 subjects with normal endoscopic retrograde cholangiopancreatography (controls), bile contained beta-carotene, alpha-carotene, lycopene, cryptoxanthin, lutein+zeaxanthin (23.9 +/- 6.6, 3.9 +/- 1.1, 39.9 +/- 21.6, 22.5 +/- 4.6, 217.1 +/- 27.8 nmol/l, respectively) with corresponding plasma values of 399.7 +/- 72.6, 88.5 +/- 18.8, 588.2 +/- 75.0, 145.1 +/- 25.9, 319.3 +/- 33.7 nmol/l. In 13 patients in whom bile duct stones impaired biliary excretion (as reflected by raised serum bilirubin), beta-carotene was significantly decreased in both plasma (199.6 +/- 35.5 nmol/l) and bile (9.4 +/- 2.0 nmol/l), with a similar trend for other carotenoids. The beta-carotene plasma/bile ratio was maintained, as well as a correlation between the two (r = 0.56; p = 0.048). Furthermore, in three subjects with complete biliary obstruction, plasma beta-carotene (35.8 +/- 20.2 nmol/l) decreased even more, probably reflecting malabsorption. In 11 patients with pancreatic diseases, plasma and bile beta-carotene were 107.9 +/- 17.8 and 6.6 +/- 2.0 nmol/l respectively, while a correlation between the two (r = 0.70; p = 0.018) again persisted, confirming the role of plasma beta-carotene in determining bile concentrations. Indeed, for the entire group (n = 41), the correlation between plasma and bile or red blood cell beta-carotene was highly significant, whereas plasma/red blood cell ratios remained unchanged. Similar findings were observed for alpha-tocopherol, with 8.4 +/- 0.9 mumol/l in control bile (vs. 23.2 +/- 1.7 mumol/l in plasma), and no significant change in the various groups. CONCLUSIONS: 1) Carotenoids and tocopherols undergo biliary excretion in man. 2) Biliary concentrations reflect plasma levels in both normal and pathologic states. 3) Decreased biliary excretion of carotenoids does not increase plasma concentrations.

Adult↗
PubMed1995

Carotenoid, retinoid and vitamin E status of the oropharyngeal mucosa in the alcoholic.

Concentrations of carotenoids, retinoids and tocopherols were determined in the homogenate of macroscopically normal appearing oropharyngeal mucosa from 10 chronic alcoholics and from 11 control patients. All the alcoholics except one had oropharyngeal cancer. No significant difference was found in tissue levels of carotenoids and tocopherols between alcoholics and controls. Furthermore, in seven of 11 controls, retinol was undetectable in the oropharyngeal mucosa, while in the alcoholics only two out of 10 had unmeasurable retinol levels. These results do not support the concept that ethanol-associated oropharyngeal carcinogenesis is due, at least in part, to local deficiencies in retinoids, carotenoids or alpha-tocopherols.

Adult↗