The Experts below are selected from a list of 222 Experts worldwide ranked by ideXlab platform
O. R. Carryl - One of the best experts on this subject based on the ideXlab platform.
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effect of pepper and Bismuth Subsalicylate on gastric pain and surface hydrophobicity in the rat
Alimentary Pharmacology & Therapeutics, 1998Co-Authors: Lenard M. Lichtenberger, O. R. Carryl, Jimmy J. Romero, Paul A. Illich, Edgar T WaltersAbstract:Background The mechanism by which dietary pepper causes dyspepsia and epigastric pain is poorly understood, as is the ability of Bismuth Subsalicylate (BSS) to relieve these symptoms. Aim To investigate the ability of black pepper, red pepper and BSS to affect gastric surface hydrophobicity and induce/relieve visceral pain in rat model systems. Methods Fasted rats were administered intragastrically Vivonex containing varying concentrations of either black or red pepper (0–200 mg/mL) and gastric contact angles were read after 1–24 h. Some rats were post-treated with BSS (2.0–17.5 mg/mL) and contact angles were read after 2–18 h. To study pain sensitivity in rats treated with pepper/BSS, we compared tail-flick latencies after the application of radiant heat. Results Both black and red pepper rapidly (< 1 h) induced a decrease in gastric surface hydrophobicity in a dose-dependent fashion. This spice-induced increase in surface wettability was long-lasting, could be enhanced in the presence of ethanol and reversed by post-treating the rats with BSS. Both black and red pepper induced an increase in pain sensitivity, consistent with the presence of gastric pain, which could also be reversed by post-treating the rats with BSS. Conclusion Both black and red pepper may induce epigastric pain by removing the stomach’s hydrophobic lining and activating intramucosal pain receptors. BSS may provide relief from postprandial dyspepsia by restoring the stomach’s non-wettable properties.
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Stress, diet and alcohol‐induced oxidative gastrointestinal mucosal injury in rats and protection by Bismuth Subsalicylate
Journal of applied toxicology : JAT, 1998Co-Authors: O. R. Carryl, Debasis Bagchi, M. X. Tran, R. L. Krohn, A. Garg, Manashi Bagchi, S. Mitra, Sidney J. StohsAbstract:Oxygen free radicals are implicated in the pathogenesis of stress and food/alcohol-induced gastrointestinal injury. We have investigated the effects of restraint stress, spicy food diet, high-fat diet and 40% ethanol on the enhanced production of reactive oxygen species, including superoxide anion and hydroxyl radicals, and on DNA fragmentation, lipid peroxidation and membrane microviscosity (indices of oxidative tissue damage) in gastric and intestinal mucosa of Sprague-Dawley rats. Furthermore, the protective ability of Bismuth Subsalicylate (BSS; 15 mg kg(−1) was determined against the gastrointestinal mucosal injury induced by these stressors. Animals on the high-fat diet consumed 31% more food as compared to other animals. Animals on the spicy food diet consumed ca. 23% more water as compared to control animals, and the high-fat diet animals consumed 17% less water. Restraint stress provided greater injury to both gastric and intestinal mucosa as compared to other stressors. Restraint stress, spicy food diet, high-fat diet and ethanol increased superoxide anion production by 10.0-, 4.3-, 5.7- and 4.8-fold, respectively, in the gastric mucosa, and by 10.4-, 5.3-, 7.0- and 5.5-fold in the intestinal mucosa. Exposure to restraint stress, spicy food diet, high-fat diet and 40% ethanol also increased hydroxyl radical production by ca. 14.3-, 4.5-, 3.5- and 4.8-fold, respectively, in the gastric mucosa, and by 17.0-, 4.8-, 3.5- and 4.7-fold in the intestinal mucosa. Bismuth Subsalicylate administration to the animals provided significant protection against superoxide anion and hydroxyl radical production. Restraint stress, spicy food diet, high-fat diet and ethanol increased lipid peroxidation by 3.6-, 2.4-, 2.6- and 2.0-fold, respectively, in the gastric mucosa, and by 4.1-, 3.5-, 3.6- and 2.7-fold in intestinal mucosa. Administration of BSS decreased restraint stress, spicy food diet, high-fat diet and ethanol-induced gastric mucosal lipid peroxidation by ca. 26%, 36%, 45% and 18%, and intestinal mucosa lipid peroxidation by 20%, 21%, 46% and 42%, respectively. Approximately 4.0-, 2.0-, 2.4- and 2.0-fold increases in DNA fragmentation were observed in the gastric mucosa of rats exposed to restraint stress, spicy food diet, high-fat diet and 40% ethanol, respectively, and similar increases in the intestinal mucosa. These same four stressors increased membrane microviscosity by 11.6-, 6.1-, 7.3- and 5.4-fold, respectively, in the gastric mucosa, and by 16.2-, 7.9-, 9.5- and 7.8-fold in the intestinal mucosa. Bismuth Subsalicylate exerted significant protection against DNA damage and changes in membrane microviscosity induced by the four stressors. Excellent correlations existed between the production of reactive oxygen species and the tissue damaging effects in both gastric and intestinal mucosa. In summary, the results demonstrate that physical and chemical stressors can induce gastrointestinal oxidative stress and mucosal injury through enhanced production of reactive oxygen species, and that BSS can significantly attenuate gastrointestinal injury by scavenging these reactive oxygen species. © 1998 John Wiley & Sons, Ltd.
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stress diet and alcohol induced oxidative gastrointestinal mucosal injury in rats and protection by Bismuth Subsalicylate
Journal of Applied Toxicology, 1998Co-Authors: O. R. Carryl, Debasis Bagchi, M. X. Tran, R. L. Krohn, A. Garg, Manashi Bagchi, S. Mitra, Sidney J. StohsAbstract:Oxygen free radicals are implicated in the pathogenesis of stress and food/alcohol-induced gastrointestinal injury. We have investigated the effects of restraint stress, spicy food diet, high-fat diet and 40% ethanol on the enhanced production of reactive oxygen species, including superoxide anion and hydroxyl radicals, and on DNA fragmentation, lipid peroxidation and membrane microviscosity (indices of oxidative tissue damage) in gastric and intestinal mucosa of Sprague-Dawley rats. Furthermore, the protective ability of Bismuth Subsalicylate (BSS; 15 mg kg(−1) was determined against the gastrointestinal mucosal injury induced by these stressors. Animals on the high-fat diet consumed 31% more food as compared to other animals. Animals on the spicy food diet consumed ca. 23% more water as compared to control animals, and the high-fat diet animals consumed 17% less water. Restraint stress provided greater injury to both gastric and intestinal mucosa as compared to other stressors. Restraint stress, spicy food diet, high-fat diet and ethanol increased superoxide anion production by 10.0-, 4.3-, 5.7- and 4.8-fold, respectively, in the gastric mucosa, and by 10.4-, 5.3-, 7.0- and 5.5-fold in the intestinal mucosa. Exposure to restraint stress, spicy food diet, high-fat diet and 40% ethanol also increased hydroxyl radical production by ca. 14.3-, 4.5-, 3.5- and 4.8-fold, respectively, in the gastric mucosa, and by 17.0-, 4.8-, 3.5- and 4.7-fold in the intestinal mucosa. Bismuth Subsalicylate administration to the animals provided significant protection against superoxide anion and hydroxyl radical production. Restraint stress, spicy food diet, high-fat diet and ethanol increased lipid peroxidation by 3.6-, 2.4-, 2.6- and 2.0-fold, respectively, in the gastric mucosa, and by 4.1-, 3.5-, 3.6- and 2.7-fold in intestinal mucosa. Administration of BSS decreased restraint stress, spicy food diet, high-fat diet and ethanol-induced gastric mucosal lipid peroxidation by ca. 26%, 36%, 45% and 18%, and intestinal mucosa lipid peroxidation by 20%, 21%, 46% and 42%, respectively. Approximately 4.0-, 2.0-, 2.4- and 2.0-fold increases in DNA fragmentation were observed in the gastric mucosa of rats exposed to restraint stress, spicy food diet, high-fat diet and 40% ethanol, respectively, and similar increases in the intestinal mucosa. These same four stressors increased membrane microviscosity by 11.6-, 6.1-, 7.3- and 5.4-fold, respectively, in the gastric mucosa, and by 16.2-, 7.9-, 9.5- and 7.8-fold in the intestinal mucosa. Bismuth Subsalicylate exerted significant protection against DNA damage and changes in membrane microviscosity induced by the four stressors. Excellent correlations existed between the production of reactive oxygen species and the tissue damaging effects in both gastric and intestinal mucosa. In summary, the results demonstrate that physical and chemical stressors can induce gastrointestinal oxidative stress and mucosal injury through enhanced production of reactive oxygen species, and that BSS can significantly attenuate gastrointestinal injury by scavenging these reactive oxygen species. © 1998 John Wiley & Sons, Ltd.
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Effect of pepper and Bismuth Subsalicylate on gastric pain and surface hydrophobicity in the rat.
Alimentary pharmacology & therapeutics, 1998Co-Authors: Lenard M. Lichtenberger, O. R. Carryl, Jimmy J. Romero, Paul A. Illich, Edgar T WaltersAbstract:Background The mechanism by which dietary pepper causes dyspepsia and epigastric pain is poorly understood, as is the ability of Bismuth Subsalicylate (BSS) to relieve these symptoms. Aim To investigate the ability of black pepper, red pepper and BSS to affect gastric surface hydrophobicity and induce/relieve visceral pain in rat model systems. Methods Fasted rats were administered intragastrically Vivonex containing varying concentrations of either black or red pepper (0–200 mg/mL) and gastric contact angles were read after 1–24 h. Some rats were post-treated with BSS (2.0–17.5 mg/mL) and contact angles were read after 2–18 h. To study pain sensitivity in rats treated with pepper/BSS, we compared tail-flick latencies after the application of radiant heat. Results Both black and red pepper rapidly (
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cytoprotective effect of Bismuth Subsalicylate in indomethacin treated rats is associated with enhanced mucus Bismuth concentration
Alimentary Pharmacology & Therapeutics, 1997Co-Authors: S. Tanaka, P. H. Guth, O. R. Carryl, Jonathan D. KaunitzAbstract:Background: Bismuth compounds prevent gastric injury from the short-term administration of nonsteroidal anti-inflammatory drugs. We studied the mechanisms underlying the gastroprotective actions of Bismuth Subsalicylate against indomethacin-induced injury in rats. Methods: An in vivo microscopic technique was used in which acid output, surface cell intracellular pH (pHi), gastric mucus gel thickness and mucosal blood flow were measured simultaneously. Concentrations of Bismuth in mucus were measured by atomic absorption. Results: Indomethacin (60 mg/kg) significantly thinned the mucus gel layer and augmented the decrease of pHi during luminal acid superfusion, consistent with a weakened gastric mucosal barrier to acid. Bismuth Subsalicylate partially reversed this effect of indomethacin on pHi, consistent with gastroprotection. Neither a prostaglandin-inhibiting but non-injurious dose of indomethacin (5 mg/kg), Bismuth Subsalicylate, or their combination affected mucus gel thickness or pHi homeostasis. In separate experiments, indomethacin (60 mg/kg) significantly increased gastric mucus Bismuth concentration in rats given Bismuth Subsalicylate. Conclusion: Bismuth accumulation in the gastric mucus during the evolution of mucosal injury may play an important role in the gastroprotective effect of Bismuth Subsalicylate against indomethacin injury.
Fabrizis L. Suarez - One of the best experts on this subject based on the ideXlab platform.
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Site of Bismuth absorption from Bismuth Subsalicylate: Implications for treatment of colonic conditions
Digestive Diseases and Sciences, 2000Co-Authors: Fabrizis L. Suarez, Julie K. Furne, Janet Stiehm, Cindy Garten, Michael LevittAbstract:Poorly absorbed Bismuth preparations may benefit a variety of chronic colonic conditions including ulcerative colitis. Bismuth-induced neurotoxicity is a potential complication of the chronic use of these preparations, and a less-absorbable form of Bismuth is needed. If Bismuth absorption occurs primarily in the upper gut, a delayed-release Bismuth preparation could reduce absorption. We studied the site of Bismuth absorption from Bismuth Subsalicylate (BSS) in rats. For 15 days, BSS (50 mg/day) was ingested or infused directly into the cecum via a chronically implanted cannula. Oral BSS resulted in serum and urine Bismuth levels many times higher (3.5 ± 0.3 μg/liter and 1570 ± 286 μg/g creatinine, respectively) than with cecal administration (undetectable (
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site of Bismuth absorption from Bismuth Subsalicylate implications for treatment of colonic conditions
Digestive Diseases and Sciences, 2000Co-Authors: Fabrizis L. Suarez, Julie K. Furne, Janet Stiehm, Cindy Garten, Michael D LevittAbstract:Poorly absorbed Bismuth preparations may benefit a variety of chronic colonic conditions including ulcerative colitis. Bismuth-induced neurotoxicity is a potential complication of the chronic use of these preparations, and a less-absorbable form of Bismuth is needed. If Bismuth absorption occurs primarily in the upper gut, a delayed-release Bismuth preparation could reduce absorption. We studied the site of Bismuth absorption from Bismuth Subsalicylate (BSS) in rats. For 15 days, BSS (50 mg/day) was ingested or infused directly into the cecum via a chronically implanted cannula. Oral BSS resulted in serum and urine Bismuth levels many times higher (3.5 ± 0.3 μg/liter and 1570 ± 286 μg/g creatinine, respectively) than with cecal administration (undetectable (<1.5 μg/liter) and 75 ± 25 μg/g creatinine). Thus, Bismuth absorption from BSS occurred almost entirely in the upper gut. These findings provide a rationale for a similar study of delayed-release Bismuth preparations in humans.
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Bismuth Subsalicylate markedly decreases hydrogen sulfide release in the human colon
Gastroenterology, 1998Co-Authors: Fabrizis L. Suarez, Julie K. Furne, John Springfield, Michael D LevittAbstract:Abstract Background & Aims: Hydrogen sulfide is one of the main malodorous compounds in human flatus. This toxic gas also has been implicated in the pathogenesis of ulcerative colitis. Therefore, a treatment that reduces colonic H 2 S levels could be clinically useful in the treatment of flatus odor and of ulcerative colitis. In this study the ability of Bismuth Subsalicylate, a compound that binds H 2 S, to reduce H 2 S release in the colon, was tested. Methods: Homogenates made from human and rat feces were incubated with and without Bismuth Subsalicylate, and gas production was measured. Fecal samples from 10 healthy subjects were analyzed before and after ingestion of Bismuth Subsalicylate (524 mg four times a day) for 3–7 days. Results: Fecal homogenates showed a dose-dependent relationship between the concentration of Bismuth Subsalicylate and H 2 S release. Treatment of subjects with Bismuth Subsalicylate produced a >95% reduction in fecal H 2 S release. Conclusions: The ability of Bismuth Subsalicylate to dramatically reduce H 2 S could provide a clinically useful means of controlling fecal and/or flatus odor and of decreasing the putative injurious effects of H 2 S on the colonic mucosa. GASTROENTEROLOGY 1998;114:923-929
Michael D Levitt - One of the best experts on this subject based on the ideXlab platform.
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site of Bismuth absorption from Bismuth Subsalicylate implications for treatment of colonic conditions
Digestive Diseases and Sciences, 2000Co-Authors: Fabrizis L. Suarez, Julie K. Furne, Janet Stiehm, Cindy Garten, Michael D LevittAbstract:Poorly absorbed Bismuth preparations may benefit a variety of chronic colonic conditions including ulcerative colitis. Bismuth-induced neurotoxicity is a potential complication of the chronic use of these preparations, and a less-absorbable form of Bismuth is needed. If Bismuth absorption occurs primarily in the upper gut, a delayed-release Bismuth preparation could reduce absorption. We studied the site of Bismuth absorption from Bismuth Subsalicylate (BSS) in rats. For 15 days, BSS (50 mg/day) was ingested or infused directly into the cecum via a chronically implanted cannula. Oral BSS resulted in serum and urine Bismuth levels many times higher (3.5 ± 0.3 μg/liter and 1570 ± 286 μg/g creatinine, respectively) than with cecal administration (undetectable (<1.5 μg/liter) and 75 ± 25 μg/g creatinine). Thus, Bismuth absorption from BSS occurred almost entirely in the upper gut. These findings provide a rationale for a similar study of delayed-release Bismuth preparations in humans.
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Bismuth Subsalicylate markedly decreases hydrogen sulfide release in the human colon
Gastroenterology, 1998Co-Authors: Fabrizis L. Suarez, Julie K. Furne, John Springfield, Michael D LevittAbstract:Abstract Background & Aims: Hydrogen sulfide is one of the main malodorous compounds in human flatus. This toxic gas also has been implicated in the pathogenesis of ulcerative colitis. Therefore, a treatment that reduces colonic H 2 S levels could be clinically useful in the treatment of flatus odor and of ulcerative colitis. In this study the ability of Bismuth Subsalicylate, a compound that binds H 2 S, to reduce H 2 S release in the colon, was tested. Methods: Homogenates made from human and rat feces were incubated with and without Bismuth Subsalicylate, and gas production was measured. Fecal samples from 10 healthy subjects were analyzed before and after ingestion of Bismuth Subsalicylate (524 mg four times a day) for 3–7 days. Results: Fecal homogenates showed a dose-dependent relationship between the concentration of Bismuth Subsalicylate and H 2 S release. Treatment of subjects with Bismuth Subsalicylate produced a >95% reduction in fecal H 2 S release. Conclusions: The ability of Bismuth Subsalicylate to dramatically reduce H 2 S could provide a clinically useful means of controlling fecal and/or flatus odor and of decreasing the putative injurious effects of H 2 S on the colonic mucosa. GASTROENTEROLOGY 1998;114:923-929
Edgar T Walters - One of the best experts on this subject based on the ideXlab platform.
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effect of pepper and Bismuth Subsalicylate on gastric pain and surface hydrophobicity in the rat
Alimentary Pharmacology & Therapeutics, 1998Co-Authors: Lenard M. Lichtenberger, O. R. Carryl, Jimmy J. Romero, Paul A. Illich, Edgar T WaltersAbstract:Background The mechanism by which dietary pepper causes dyspepsia and epigastric pain is poorly understood, as is the ability of Bismuth Subsalicylate (BSS) to relieve these symptoms. Aim To investigate the ability of black pepper, red pepper and BSS to affect gastric surface hydrophobicity and induce/relieve visceral pain in rat model systems. Methods Fasted rats were administered intragastrically Vivonex containing varying concentrations of either black or red pepper (0–200 mg/mL) and gastric contact angles were read after 1–24 h. Some rats were post-treated with BSS (2.0–17.5 mg/mL) and contact angles were read after 2–18 h. To study pain sensitivity in rats treated with pepper/BSS, we compared tail-flick latencies after the application of radiant heat. Results Both black and red pepper rapidly (< 1 h) induced a decrease in gastric surface hydrophobicity in a dose-dependent fashion. This spice-induced increase in surface wettability was long-lasting, could be enhanced in the presence of ethanol and reversed by post-treating the rats with BSS. Both black and red pepper induced an increase in pain sensitivity, consistent with the presence of gastric pain, which could also be reversed by post-treating the rats with BSS. Conclusion Both black and red pepper may induce epigastric pain by removing the stomach’s hydrophobic lining and activating intramucosal pain receptors. BSS may provide relief from postprandial dyspepsia by restoring the stomach’s non-wettable properties.
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Effect of pepper and Bismuth Subsalicylate on gastric pain and surface hydrophobicity in the rat.
Alimentary pharmacology & therapeutics, 1998Co-Authors: Lenard M. Lichtenberger, O. R. Carryl, Jimmy J. Romero, Paul A. Illich, Edgar T WaltersAbstract:Background The mechanism by which dietary pepper causes dyspepsia and epigastric pain is poorly understood, as is the ability of Bismuth Subsalicylate (BSS) to relieve these symptoms. Aim To investigate the ability of black pepper, red pepper and BSS to affect gastric surface hydrophobicity and induce/relieve visceral pain in rat model systems. Methods Fasted rats were administered intragastrically Vivonex containing varying concentrations of either black or red pepper (0–200 mg/mL) and gastric contact angles were read after 1–24 h. Some rats were post-treated with BSS (2.0–17.5 mg/mL) and contact angles were read after 2–18 h. To study pain sensitivity in rats treated with pepper/BSS, we compared tail-flick latencies after the application of radiant heat. Results Both black and red pepper rapidly (
Debasis Bagchi - One of the best experts on this subject based on the ideXlab platform.
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Stress, diet and alcohol‐induced oxidative gastrointestinal mucosal injury in rats and protection by Bismuth Subsalicylate
Journal of applied toxicology : JAT, 1998Co-Authors: O. R. Carryl, Debasis Bagchi, M. X. Tran, R. L. Krohn, A. Garg, Manashi Bagchi, S. Mitra, Sidney J. StohsAbstract:Oxygen free radicals are implicated in the pathogenesis of stress and food/alcohol-induced gastrointestinal injury. We have investigated the effects of restraint stress, spicy food diet, high-fat diet and 40% ethanol on the enhanced production of reactive oxygen species, including superoxide anion and hydroxyl radicals, and on DNA fragmentation, lipid peroxidation and membrane microviscosity (indices of oxidative tissue damage) in gastric and intestinal mucosa of Sprague-Dawley rats. Furthermore, the protective ability of Bismuth Subsalicylate (BSS; 15 mg kg(−1) was determined against the gastrointestinal mucosal injury induced by these stressors. Animals on the high-fat diet consumed 31% more food as compared to other animals. Animals on the spicy food diet consumed ca. 23% more water as compared to control animals, and the high-fat diet animals consumed 17% less water. Restraint stress provided greater injury to both gastric and intestinal mucosa as compared to other stressors. Restraint stress, spicy food diet, high-fat diet and ethanol increased superoxide anion production by 10.0-, 4.3-, 5.7- and 4.8-fold, respectively, in the gastric mucosa, and by 10.4-, 5.3-, 7.0- and 5.5-fold in the intestinal mucosa. Exposure to restraint stress, spicy food diet, high-fat diet and 40% ethanol also increased hydroxyl radical production by ca. 14.3-, 4.5-, 3.5- and 4.8-fold, respectively, in the gastric mucosa, and by 17.0-, 4.8-, 3.5- and 4.7-fold in the intestinal mucosa. Bismuth Subsalicylate administration to the animals provided significant protection against superoxide anion and hydroxyl radical production. Restraint stress, spicy food diet, high-fat diet and ethanol increased lipid peroxidation by 3.6-, 2.4-, 2.6- and 2.0-fold, respectively, in the gastric mucosa, and by 4.1-, 3.5-, 3.6- and 2.7-fold in intestinal mucosa. Administration of BSS decreased restraint stress, spicy food diet, high-fat diet and ethanol-induced gastric mucosal lipid peroxidation by ca. 26%, 36%, 45% and 18%, and intestinal mucosa lipid peroxidation by 20%, 21%, 46% and 42%, respectively. Approximately 4.0-, 2.0-, 2.4- and 2.0-fold increases in DNA fragmentation were observed in the gastric mucosa of rats exposed to restraint stress, spicy food diet, high-fat diet and 40% ethanol, respectively, and similar increases in the intestinal mucosa. These same four stressors increased membrane microviscosity by 11.6-, 6.1-, 7.3- and 5.4-fold, respectively, in the gastric mucosa, and by 16.2-, 7.9-, 9.5- and 7.8-fold in the intestinal mucosa. Bismuth Subsalicylate exerted significant protection against DNA damage and changes in membrane microviscosity induced by the four stressors. Excellent correlations existed between the production of reactive oxygen species and the tissue damaging effects in both gastric and intestinal mucosa. In summary, the results demonstrate that physical and chemical stressors can induce gastrointestinal oxidative stress and mucosal injury through enhanced production of reactive oxygen species, and that BSS can significantly attenuate gastrointestinal injury by scavenging these reactive oxygen species. © 1998 John Wiley & Sons, Ltd.
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stress diet and alcohol induced oxidative gastrointestinal mucosal injury in rats and protection by Bismuth Subsalicylate
Journal of Applied Toxicology, 1998Co-Authors: O. R. Carryl, Debasis Bagchi, M. X. Tran, R. L. Krohn, A. Garg, Manashi Bagchi, S. Mitra, Sidney J. StohsAbstract:Oxygen free radicals are implicated in the pathogenesis of stress and food/alcohol-induced gastrointestinal injury. We have investigated the effects of restraint stress, spicy food diet, high-fat diet and 40% ethanol on the enhanced production of reactive oxygen species, including superoxide anion and hydroxyl radicals, and on DNA fragmentation, lipid peroxidation and membrane microviscosity (indices of oxidative tissue damage) in gastric and intestinal mucosa of Sprague-Dawley rats. Furthermore, the protective ability of Bismuth Subsalicylate (BSS; 15 mg kg(−1) was determined against the gastrointestinal mucosal injury induced by these stressors. Animals on the high-fat diet consumed 31% more food as compared to other animals. Animals on the spicy food diet consumed ca. 23% more water as compared to control animals, and the high-fat diet animals consumed 17% less water. Restraint stress provided greater injury to both gastric and intestinal mucosa as compared to other stressors. Restraint stress, spicy food diet, high-fat diet and ethanol increased superoxide anion production by 10.0-, 4.3-, 5.7- and 4.8-fold, respectively, in the gastric mucosa, and by 10.4-, 5.3-, 7.0- and 5.5-fold in the intestinal mucosa. Exposure to restraint stress, spicy food diet, high-fat diet and 40% ethanol also increased hydroxyl radical production by ca. 14.3-, 4.5-, 3.5- and 4.8-fold, respectively, in the gastric mucosa, and by 17.0-, 4.8-, 3.5- and 4.7-fold in the intestinal mucosa. Bismuth Subsalicylate administration to the animals provided significant protection against superoxide anion and hydroxyl radical production. Restraint stress, spicy food diet, high-fat diet and ethanol increased lipid peroxidation by 3.6-, 2.4-, 2.6- and 2.0-fold, respectively, in the gastric mucosa, and by 4.1-, 3.5-, 3.6- and 2.7-fold in intestinal mucosa. Administration of BSS decreased restraint stress, spicy food diet, high-fat diet and ethanol-induced gastric mucosal lipid peroxidation by ca. 26%, 36%, 45% and 18%, and intestinal mucosa lipid peroxidation by 20%, 21%, 46% and 42%, respectively. Approximately 4.0-, 2.0-, 2.4- and 2.0-fold increases in DNA fragmentation were observed in the gastric mucosa of rats exposed to restraint stress, spicy food diet, high-fat diet and 40% ethanol, respectively, and similar increases in the intestinal mucosa. These same four stressors increased membrane microviscosity by 11.6-, 6.1-, 7.3- and 5.4-fold, respectively, in the gastric mucosa, and by 16.2-, 7.9-, 9.5- and 7.8-fold in the intestinal mucosa. Bismuth Subsalicylate exerted significant protection against DNA damage and changes in membrane microviscosity induced by the four stressors. Excellent correlations existed between the production of reactive oxygen species and the tissue damaging effects in both gastric and intestinal mucosa. In summary, the results demonstrate that physical and chemical stressors can induce gastrointestinal oxidative stress and mucosal injury through enhanced production of reactive oxygen species, and that BSS can significantly attenuate gastrointestinal injury by scavenging these reactive oxygen species. © 1998 John Wiley & Sons, Ltd.