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Eight groups of 5 rats were fed 8 differing liquid diets with and without ethanol, cod liver oil and/or increased levels of vitamin E. Hepatic levels of vitamins A and E were determined following the 28-day feeding time. Ethanol... more
Eight groups of 5 rats were fed 8 differing liquid diets with and without ethanol, cod liver oil and/or increased levels of vitamin E. Hepatic levels of vitamins A and E were determined following the 28-day feeding time. Ethanol consumption decreased the levels of hepatic vitamin E (p less than 0.05), vitamin A (p less than 0.05) and the ratio of vitamin A/E (p less than 0.05). Hepatic levels of vitamins A and E were unaffected in rats fed cod liver oil. Supplementation of the normal dietary level of 30 IU of vitamin E per kg diet, with an additional 142 IU alpha tocopherol/kg diet, restored hepatic concentrations of vitamin E to normal levels in alcohol-fed rats. The hepatic levels of vitamin A in rats fed ethanol diets supplemented with vitamin E were less than that of control rats but were 4.3 times greater than that of rats on ethanol diets unsupplemented with vitamin E. However, the vitamin A and E ratio was equal to normal in this group of rats. The vitamin A/E ratio was reduced in liver of rats fed non-alcoholic diets supplemented with vitamin E due to increased levels of hepatic vitamin E. Additionally, rats fed cod liver oil diets containing ethanol also indicated decreased hepatic vitamin A and E levels. However, these levels were greater than that of rats fed only alcoholic diets suggesting that these vitamins are replaced by the vitamin A and E content in the cod liver oil.(ABSTRACT TRUNCATED AT 250 WORDS)
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▪ More than one million Americans were expected to be diagnosed with cancer in 2003 ( 7a ). Compelling experimental, epidemiological, and clinical evidence indicates that many cancers are preventable, especially because diet and... more
▪ More than one million Americans were expected to be diagnosed with cancer in 2003 ( 7a ). Compelling experimental, epidemiological, and clinical evidence indicates that many cancers are preventable, especially because diet and nutrition are key factors in the modulation of cancer risk. The road to nutritional intervention in cancer prevention has led to successful trials as well as trials that did not reach their intended endpoints. This chapter reviews four case studies of trials, with two ending in success and two ending in null findings or adverse effects. The goal is to identify lessons learned from all four case studies and from the investigations of the complexities inherent to nutritional intervention trials. Additional insights are presented by the research addressing potential mechanisms underlying the endpoints of human trials. Future progress in nutrition and cancer prevention will require expertise from multidisciplinary teams to develop new knowledge about specific ...
Research Interests: Nutrition and Dietetics, Nutrition, Clinical Trial, Cancer, Diet, and 12 moreCancer Prevention, Medicine, Humans, Case Study, Lessons Learned, Neoplasms, Multidisciplinary Teams, Guidance and Counseling Intervention Programs, Multidisciplinary Approach, Cancer Risk, Randomized Controlled Trials as Topic, and Adverse effect
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In bacteriophage T 4 , temperature-sensitive (ts) mutations in gene 32 as well as in gene 43 have previously been shown to stimulate reversion of frame-shift mutations. We show here that twots mutations in gene 32 increase reversion of... more
In bacteriophage T 4 , temperature-sensitive (ts) mutations in gene 32 as well as in gene 43 have previously been shown to stimulate reversion of frame-shift mutations. We show here that twots mutations in gene 32 increase reversion of base substitution mutations.ts mutations in ...
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Alcohol is a major cancer risk factor. A variety of roles in carcinogenesis have been assigned to ethanol. Our recent studies indicate that ethanol may act as tumor promoter. Further studies suggest that ethanol may act as tumor promoter... more
Alcohol is a major cancer risk factor. A variety of roles in carcinogenesis have been assigned to ethanol. Our recent studies indicate that ethanol may act as tumor promoter. Further studies suggest that ethanol may act as tumor promoter through free radicals generated during its metabolism because an increase in tumors was observed under conditions in which ethanol-induced lipid peroxidation could take place and not in which such lipid peroxidation could not occur. Other possibilities include ethanol effect on cell necrosis and cell proliferation and generation of a secondary mutagenic event through a DNA repair deficiency. The immune system, because it is a defense mechanism against carcinogenesis and because ethanol is immunosuppressive, must also play a role. Our current studies are aimed at elucidating some of these mechanisms and pointing out the complexity of the mechanisms that are affected by ethanol and that may be involved in tumor promotion.
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Seventy-five percent of esophageal cancers are alcohol related, yet alcohol is not a carcinogen. Ethanol may promote carcinogenesis via increased free radical products during its metabolism, as indicated by data from this and other... more
Seventy-five percent of esophageal cancers are alcohol related, yet alcohol is not a carcinogen. Ethanol may promote carcinogenesis via increased free radical products during its metabolism, as indicated by data from this and other studies. Ethanol is oxidized to acetaldehyde by alcohol dehydrogenase, catalase and the microsomal ethanol oxidizing system (MEOS). Free radicals (FR) are released during the oxidation of ethanol by the MEOS. An increased formation of FR in tissues would increase their oxidative stress and may increase their susceptibility for developing chemically induced cancers. FR and some FR products can rapidly react with biological materials, i.e. lipids, proteins and nucleic acids, forming toxic products. This study focuses on the effects of FR and/or FR products on cancer promotion during alcohol metabolism. Eight groups of mice were fed nutritionally adequate diets supplemented with vitamin E and/or ethanol. Some groups of mice were also orally gavaged with N-nitrosomethylbenzylamine (NMBzA), an esophageal carcinogen. Following the feeding of the various diets for 22 weeks, livers and esophagi were removed and the FR burden in the liver measured by the presence of lipid peroxide products and the number of tumors in each esophagus determined. These studies indicate that a linear relationship exists between the increasing number of esophageal tumors and increasing levels of lipid peroxide products that are formed during FR activity. These results show that FR and/or FR products are the cancer promoters during ethanol metabolism, since diets supplemented with high levels of vitamin E, which inhibits ethanol-induced FR activity and the formation of FR products, suppress the promotion of cancer by ethanol.(ABSTRACT TRUNCATED AT 250 WORDS)
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Neoplastic development in the esophagus is characterized by abnormal activity in the basal cell proliferative compartment. Malignancy starts with mild dysplasia. Barrett's esophagus is associated with columnar epithelial dysplasia and... more
Neoplastic development in the esophagus is characterized by abnormal activity in the basal cell proliferative compartment. Malignancy starts with mild dysplasia. Barrett's esophagus is associated with columnar epithelial dysplasia and presents increased risk for adenocarcinoma. Esophagitis, especially with chronicity, may constitute a predisposing characteristic in high incidence areas. This paper briefly describes the main features of precancerous lesions in the esophagus. It then focuses on a discussion of the biological markers of malignancy in the oral cavity and esophagus that are currently under study. Such biomarkers include promising differentiation markers such as keratins, involucrin, particulate transglutaminase, as well as growth factors, and most studied but nonspecific onco-developmental markers, e.g., carcinoembryonic antigen, alpha 1-fetaprotein, hormone/enzyme markers, e.g., human chorionic gonadotropin and placental lactogen, and a number of other miscellaneous...
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... cytokines (Tilg et al., 1992). McClain et al. (1993) were able to demonstrate that serum levels of IL-1, IL-6, IL-8 and TNF are increased in patients with alcoholic liver disease.Earnest et al. (1993) demonstrated that Kupffer cells ...
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Promotion of chemically induced esophageal cancer by ethanol may include the generation of highly reactive free radicals and thus may be preventable by the antioxidant vitamin E. In the present study, female C57BL/6 mice received... more
Promotion of chemically induced esophageal cancer by ethanol may include the generation of highly reactive free radicals and thus may be preventable by the antioxidant vitamin E. In the present study, female C57BL/6 mice received N-nitrosomethylbenzylamine (NMBzA, 0.2 mg/kg ig) three times a week for three weeks. After this esophageal carcinogenic treatment, mice were fed a nutritionally adequate liquid diet with 30% of the calories supplied by ethanol or an isocaloric carbohydrate with or without supplemental alpha-tocopherol (142 mg/kg diet). As a marker of in vivo lipid peroxidation, exhaled ethane was collected and measured 24 hours "before" the mice were killed after 20 weeks of dietary treatment. Hepatic malondialdehyde, lipid fluorescence, and conjugated dienes were determined as markers of products of lipid peroxidation and serum aminotransferases as indexes of liver toxicity. Hepatic liver concentrations of vitamins A and E and the size and frequency of esophageal tumors were also assessed. Ethanol consumption after NMBzA administration significantly increased (p less than 0.05) the size and frequency of esophageal tumors. These ethanol-promoted effects were accompanied by increases in indexes of in vivo and accumulated products of lipid peroxidation. Similarly treated animals that received supplemental dietary vitamin E showed significant reductions (p less than 0.05) in mean tumor size and frequency of tumors as well as a decrease in the indexes of hepatic lipid peroxidation. The results suggest that promotion of NMBzA-induced esophageal tumors by ethanol may in part result from increased lipid peroxidation and that vitamin E reduces carcinogenicity of NMBzA or ethanol promoter effects by inhibiting lipid peroxidation.
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Pouches of male Syrian Golden hamsters were painted with 1% 7,12-dimethylbenz[a]anthracene (DMBA) three times for one week. One week after DMBA treatment, hamsters were fed an ethanolic diet and continued on this diet until they were... more
Pouches of male Syrian Golden hamsters were painted with 1% 7,12-dimethylbenz[a]anthracene (DMBA) three times for one week. One week after DMBA treatment, hamsters were fed an ethanolic diet and continued on this diet until they were killed 22 and 35 weeks after the start of the experiment. Phospholipids, cholesterol, indexes of lipid peroxidation (malondialdehyde, diene and triene conjugates, lipid fluorescence), and the antioxidants glutathione and vitamin E were determined in the buccal mucosa, as was the incidence of tumors. At 22 weeks, the relative proportion of cholesterol to phospholipids in ethanol-consuming hamsters was significantly increased. At 35 weeks, most of the treatments showed a return of cholesterol vs. phospholipids toward that of untreated mucosa at 22 weeks. Ethanol consumption also increased the indexes of lipid peroxidation at 22 weeks; the largest increases occurred when ethanol use was combined with DMBA treatment. However, at 35 weeks such increases in lipid peroxidation had either returned to intermediate levels or were not different from the untreated controls at 22 weeks. Glutathione decreased in pouches of hamsters fed ethanol diets at 22 weeks, but at 35 weeks there was no appreciable difference. However, vitamin E increased significantly with ethanol consumption at 22 weeks, which increased further when combined with DMBA treatment, but at 35 weeks these values were intermediate. No tumors were seen at 22 weeks. At 35 weeks, DMBA-treated ethanol-fed hamsters had a significantly higher incidence of tumors, more multiple tumors per hamster with tumors, and more of the larger tumors than DMBA-treated control-fed hamsters. The results suggest that an increase in lipid peroxidation occurs with ethanol-related tumor promotion processes, but this lipid peroxidation declines when tumors appear to be preceded by increases in cholesterol relative to phospholipids and increases in vitamin E.
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Tumor appearance can be accelerated in the immunodeficient and immunosuppressed animal. The role of lipid peroxidation and immune dysfunction induced by retrovirus and ethanol treatments on cancer promotion were investigated. Following... more
Tumor appearance can be accelerated in the immunodeficient and immunosuppressed animal. The role of lipid peroxidation and immune dysfunction induced by retrovirus and ethanol treatments on cancer promotion were investigated. Following the initiation of esophageal cancer by methylbenzylnitrosamine, ethanol consumption and retrovirus infection individually and concomitantly increased growth of esophageal tumors. Dietary supplementation with vitamin E reduced the size and frequency of the developed tumors. Tumor growth modifications in the vitamin E supplemented animals may be due to changes in T-cell numbers and functions stimulated by vitamin E. In addition, increased production of free radicals following ethanol treatment and retrovirus infection, and the suppression of these formations lipid peroxide by vitamin E is accompanied by lower incidence and size of tumors. Thus, the mechanisms of tumor enhancement observed in immunocompromised animals may include a combination of immunomodulation and modification of oxidant production by ethanol consumption and retrovirus infection.
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Ethanol was found to alter functioning and numbers of lymphoid cells of the cellular immune system in humans and rats. In in-vitro studies on human lymphocytes, a higher than 0.1% concentration of ethanol and acetaldehyde and acetic acid,... more
Ethanol was found to alter functioning and numbers of lymphoid cells of the cellular immune system in humans and rats. In in-vitro studies on human lymphocytes, a higher than 0.1% concentration of ethanol and acetaldehyde and acetic acid, the metabolites of ethanol, caused a decrease in the formation of E-rosettes. Methanol and propanol also resulted in a decrease in E-rosette formation. The natural killer (NK) cells varied in their ability to lyse tumor cells. In vitro, the NK-cell activity declined at higher than 0.2% concentration of ethanol. The NK activity in cells isolated from spleen and thymus of rats fed 1 g/dl or 7 g/dl ethanol did not differ significantly from the controls. Sprague Dawley rats fed 1 g/dl or 7 g/dl ethanol for 12 weeks had a significantly smaller thymus compared to the controls. Alveolar macrophages isolated from the rats exhibited impaired phagocytic activity. In agreement with other investigators, ethanol was found to result in a loss of T-cell population in the spleens of rats fed ethanol for 13 months. On the other hand, the T-helper cells and the proportion of T-helper to T-suppressor cells were found to increase in the splenocytes from these rats. This latter occurrence, apparently, is to compensate for the general loss of T-cell population observed in the body that occurs with ethanol ingestion. It is hypothesized that immunosuppression and the transient imbalances in the components of the cellular immunity induced by ethanol lead to an increased risk of pathogenesis associated with alcohol consumption.
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... All rights reserved.VITAMIN E ATTENUATION OF THE EFFECTS OF CHRONIC ETHANOL AND COD LIVER OIL CONSUMPTION ON RAT LIVER LIPID COMPOSITION Olalekan E. Odeleye,1'4 Cleamond D. Eskelson,TM Siraj I. Mufti~ and Ronald R. Watson1,4 ...... more
... All rights reserved.VITAMIN E ATTENUATION OF THE EFFECTS OF CHRONIC ETHANOL AND COD LIVER OIL CONSUMPTION ON RAT LIVER LIPID COMPOSITION Olalekan E. Odeleye,1'4 Cleamond D. Eskelson,TM Siraj I. Mufti~ and Ronald R. Watson1,4 ... Carroll KK. ...
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Promotion of chemically induced esophageal cancer by ethanol may include the generation of highly reactive free radicals and thus may be preventable by the antioxidant vitamin E. In the present study, female C57BL/6 mice received... more
Promotion of chemically induced esophageal cancer by ethanol may include the generation of highly reactive free radicals and thus may be preventable by the antioxidant vitamin E. In the present study, female C57BL/6 mice received N-nitrosomethylbenzylamine (NMBzA, 0.2 mg/kg ig) three times a week for three weeks. After this esophageal carcinogenic treatment, mice were fed a nutritionally adequate liquid diet with 30% of the calories supplied by ethanol or an isocaloric carbohydrate with or without supplemental alpha-tocopherol (142 mg/kg diet). As a marker of in vivo lipid peroxidation, exhaled ethane was collected and measured 24 hours "before" the mice were killed after 20 weeks of dietary treatment. Hepatic malondialdehyde, lipid fluorescence, and conjugated dienes were determined as markers of products of lipid peroxidation and serum aminotransferases as indexes of liver toxicity. Hepatic liver concentrations of vitamins A and E and the size and frequency of esophageal tumors were also assessed. Ethanol consumption after NMBzA administration significantly increased (p less than 0.05) the size and frequency of esophageal tumors. These ethanol-promoted effects were accompanied by increases in indexes of in vivo and accumulated products of lipid peroxidation. Similarly treated animals that received supplemental dietary vitamin E showed significant reductions (p less than 0.05) in mean tumor size and frequency of tumors as well as a decrease in the indexes of hepatic lipid peroxidation. The results suggest that promotion of NMBzA-induced esophageal tumors by ethanol may in part result from increased lipid peroxidation and that vitamin E reduces carcinogenicity of NMBzA or ethanol promoter effects by inhibiting lipid peroxidation.
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Pouches of male Syrian Golden hamsters were painted with 1% 7,12-dimethylbenz[a]anthracene (DMBA) three times for one week. One week after DMBA treatment, hamsters were fed an ethanolic diet and continued on this diet until they were... more
Pouches of male Syrian Golden hamsters were painted with 1% 7,12-dimethylbenz[a]anthracene (DMBA) three times for one week. One week after DMBA treatment, hamsters were fed an ethanolic diet and continued on this diet until they were killed 22 and 35 weeks after the start of the experiment. Phospholipids, cholesterol, indexes of lipid peroxidation (malondialdehyde, diene and triene conjugates, lipid fluorescence), and the antioxidants glutathione and vitamin E were determined in the buccal mucosa, as was the incidence of tumors. At 22 weeks, the relative proportion of cholesterol to phospholipids in ethanol-consuming hamsters was significantly increased. At 35 weeks, most of the treatments showed a return of cholesterol vs. phospholipids toward that of untreated mucosa at 22 weeks. Ethanol consumption also increased the indexes of lipid peroxidation at 22 weeks; the largest increases occurred when ethanol use was combined with DMBA treatment. However, at 35 weeks such increases in lipid peroxidation had either returned to intermediate levels or were not different from the untreated controls at 22 weeks. Glutathione decreased in pouches of hamsters fed ethanol diets at 22 weeks, but at 35 weeks there was no appreciable difference. However, vitamin E increased significantly with ethanol consumption at 22 weeks, which increased further when combined with DMBA treatment, but at 35 weeks these values were intermediate. No tumors were seen at 22 weeks. At 35 weeks, DMBA-treated ethanol-fed hamsters had a significantly higher incidence of tumors, more multiple tumors per hamster with tumors, and more of the larger tumors than DMBA-treated control-fed hamsters. The results suggest that an increase in lipid peroxidation occurs with ethanol-related tumor promotion processes, but this lipid peroxidation declines when tumors appear to be preceded by increases in cholesterol relative to phospholipids and increases in vitamin E.
Research Interests: Nutrition and Dietetics, Phospholipids, Cholesterol, Animals, Male, and 14 moreGlutathione, Ethanol, Vitamin E, Lipid peroxidation, Nutrition and Cancer, Topical Drug Administration, Mouth Neoplasms, Mouth mucosa, Oxidation-Reduction, Malondialdehyde, Lipid Biochemsitry and environmental toxicants, Cheek, Cricetinae, and Drug synergism
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Research Interests: Free Radicals, Cell Division, Free Radical, Humans, Mice, and 9 moreAlcoholism, Female, Animals, Male, Ethanol, Risk factors, Rats, Necrosis, and Risk Factors
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Preliminary dose finding studies showed that 22 mg/kg of N-nitrosomethylbenzylamine (NMBZA) delivered over 5 days did not induce esophageal lesions, but 18 mg/kg administered over a period of 2 or 3 weeks did induce these lesions. Based... more
Preliminary dose finding studies showed that 22 mg/kg of N-nitrosomethylbenzylamine (NMBZA) delivered over 5 days did not induce esophageal lesions, but 18 mg/kg administered over a period of 2 or 3 weeks did induce these lesions. Based on these results, Sprague-Dawley rats were treated with 2.5 mg/kg NMBZA three times a week for 3 weeks to initiate esophageal carcinogenesis. The experimental animals were administered isocaloric ethanol diet either before and during NMBZA initiated carcinogenesis, or after initiation as a tumor promoter. The esophagi of rats that died or who were terminated at 18 months of age were examined for nodules and tumors. When ethanol was administered before and during initiation, the mean frequency of esophageal lesions was 8.04 +/- 3.04/rat with an average size of 1.44 +/- 0.27 mm versus 12.41 +/- 2.12/rat and 0.92 +/- 0.17 mm respectively for the controls. Only three out of 13 of the ethanol-fed rats had tumors (mainly squamous papillomas) versus 10 out of 26 of the control-fed animals. Ethanol consumption before and during initiation, therefore, decreased the incidence of esophageal nodules and tumors. With ethanol administered as a promoter, on the other hand, while incidence of the total lesions was not affected appreciably, the incidence of tumors was remarkably increased. With ethanol promotion the mean frequency of lesions was 8.75 +/- 1.07/rat with an average size of 1.02 +/- 0.09 mm versus 10.94 +/- 1.49/rat and 1.32 +/- 0.13 mm respectively for the controls. In this case, the ethanol-consuming rats had tumors in 14 out of 75 animals versus one small tumor in 32 of the controls. The results indicate that the occurrence of esophageal tumors is inhibited by simultaneous ethanol administration, but promoted when ethanol is administered post-initiation ostensibly by allowing extensive dysplastic proliferation of the carcinogen-induced lesions.
Research Interests: Animals, Male, Ethanol, Carcinogens, Carcinogenesis, and 3 moreRats, Time Factors, and Dimethylnitrosamine
Page 1. Carcinogeneds vol.13 no.10 pp.1811 1816, 1992 Vitamin E protection against nitrosamine-induced esophageal tumor incidence in mice immunocompromised by retroviral infection Olalekan E.Odeleye, Cleamond D.Eskelson1, Siraj I.Mufti2... more
Page 1. Carcinogeneds vol.13 no.10 pp.1811 1816, 1992 Vitamin E protection against nitrosamine-induced esophageal tumor incidence in mice immunocompromised by retroviral infection Olalekan E.Odeleye, Cleamond D.Eskelson1, Siraj I.Mufti2 and Ronald R.Watson3 ...
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Alcohol is a major risk factor for cancers of the upper gastrointestinal tract but the association with cancers of the large bowel is not as clearly established. In recent studies, we have provided experimental support for the... more
Alcohol is a major risk factor for cancers of the upper gastrointestinal tract but the association with cancers of the large bowel is not as clearly established. In recent studies, we have provided experimental support for the associations in the esophagus and oral cavity. Our studies also indicate that the tumor promotion ability of ethanol is related to its ability to generate oxygen free radicals as measured by an increase in indices of lipid peroxidation. This increase in lipid peroxidation was evident in the liver as well as the tissues targeted by the site-specific carcinogens and promoted by ethanol. Studies in mice showed that the increased lipid peroxidation as well as tumor incidence was inhibited by the administration of vitamin E, the potent antioxidant. Determination of fatty acid profiles showed significant alterations when ethanol was used as a tumor promoter after treatment with the carcinogen. Ethanol as a promoter caused an increase in esophageal polyunsaturated fatty acids (PUFA). Ethanol promotion was also evident in increased arachidonate and an exaggeration in PUFA that are involved in eicosanoid production. Thus, these results suggest that ethanol-related promotion may be the result of excessive cell proliferation induced by disordered lipid and eicosanoid metabolism that may cause a selective outgrowth of the carcinogen-initiated cells. Supporting evidence for ethanol-induced hyper-regeneration is also reviewed.
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Research Interests: Multidisciplinary, Vitamin A, Liver, Mice, Female, and 5 moreAnimals, Ethanol, Vitamin E, Carcinogens, and Dimethylnitrosamine
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VASANTHI NACHIAPPAN,* SIRAJ I. MUFn,*tt. AGNISH CHAKRAVARTI,* CLEAMOND D. ESKELSON§ and RAM RAJASEKHARAN* ... Departments of 'Pharmacology and Toxicology, and jSurgery, and tthe Arizona Cancer Center, University of Arizona, Tucson, ...
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Research Interests: Psychology, Free Radicals, Phospholipids, Fatty acids, Reactive Oxygen Species, and 15 moreAlcohol, Alcoholism, Animals, Male, Glutathione, Ethanol, Vitamin E, Carcinogens, Lipid peroxidation, Rats, Esophagus, Public health systems and services research, Neurosciences, Dimethylnitrosamine, and Malondialdehyde
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We discuss evidence indicating how ethanol could generate oxygen free radicals. Recent use of techniques such as spin trapping and EPR spectroscopy have demonstrably confirmed that both acute and chronic alcohol use by laboratory animals... more
We discuss evidence indicating how ethanol could generate oxygen free radicals. Recent use of techniques such as spin trapping and EPR spectroscopy have demonstrably confirmed that both acute and chronic alcohol use by laboratory animals would generate free radical intermediates. These radicals are of biological origin and presumably involve lipids. However, an exact identification of the intermediates produced has not been worked out with the currently available methodologies. Also not known is the mechanism whereby ethanol could initiate free radicals. The relationship between generation of free radicals and cell toxicity or carcinogenesis is also not understood. Using a variety of systems that included different species, strains and gender (male Sprague-Dawley and Fisher-344 rats, female C57BL/6 mice, male Syrian golden hamsters) and carcinogens (NMBZA, NNN, NNK, DMBA and LP-BM5 retrovirus) we have shown an association of lipid peroxidation with ethanol tumor promotionability. Ho...