ascorbic-acid and Intestinal-Diseases

Radiation-induced gastrointestinal injury or radiation enteropathy is an imminent risk during radiation therapy of abdominal or pelvic tumors. Despite remarkable technological advancements in image-guided radiation delivery techniques, the risk of intestinal injury after radiotherapy for abdominal or pelvic cancers has not been completely eliminated. The irradiated intestine undergoes varying degrees of adverse structural and functional changes, which can result in transient or long-term complications. The risk of development of enteropathy depends on dose, fractionation, and quality of radiation. Moreover, the patients' medical condition, age, inter-individual sensitivity to radiation and size of the treatment area are also risk factors of radiation enteropathy. Therefore, strategies are needed to prevent radiotherapy-induced undesirable alteration in the gastrointestinal tract. Many natural plant products, by virtue of their plethora of biological activities, alleviate the adverse effects of radiation-induced injury. The current review discusses potential roles and possible mechanisms of natural plant products in suppressing radiation enteropathy. Natural plant products have the potential to suppress intestinal radiation toxicity.

Topics: Abdominal Neoplasms; Ascorbic Acid; Biological Products; Curcumin; Garlic; Humans; Intestinal Diseases; Pelvic Neoplasms; Plant Extracts; Radiation Injuries; Vitamin E

Intestinal type metaplasia plays a role in intestinal type gastric carcinoma development. Ascorbic acid demonstrates a protective effect against gastric carcinogenesis, due to its ability to inactivate oxygen free-radicals as well as its nitrite-scavenging effects.. To assess whether long-term ascorbic acid administration following Helicobacter pylori eradication could affect intestinal metaplasia regression in the stomach.. Sixty-five patients were included in the study. The inclusion criterion was the presence of intestinal metaplasia on the gastric mucosa after H. pylori eradication. An upper gastrointestinal endoscopy was performed and 3 biopsy specimens were taken in the antrum, 3 in the gastric body, and 2 in the incisura angularis. Patients were randomized to receive 500 mg of ascorbic acid o.d., after lunch (32 patients) for 6 months or no treatment (33 patients). All patients underwent to endoscopic control at the end of the 6 months.. H. pylori infection recurrence was detected in 6 (9.4%) patients (three from each group), and these patients were excluded from further analysis. We were unable to find evidence of intestinal metaplasia in any biopsied site of the gastric mucosa in 9/29 (31%) patients from the ascorbic acid group and in 1/29 (3.4%) of the patients from the control group (P=0.006). Moreover, a further six (20.7%) patients from the ascorbic acid group presenting chronic inactive pangastritis with widespread intestinal metaplasia at entry, showed less extensive antritis with intestinal metaplasia at control, whilst a similar finding was only seen in one patient from the control group (P=0.051).. The administration of ascorbic acid significantly helps to resolve intestinal metaplasia of the gastric mucosa following H. pylori eradication, and its use as a chemoprevention treatment should be considered.

Topics: Adult; Aged; Ascorbic Acid; Female; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Diseases; Male; Metaplasia; Middle Aged; Prospective Studies; Recurrence; Stomach Diseases

This study was aimed at investigating morphological and biochemical efficacies of antioxidants on indomethacin-induced small intestinal damage in rats. Group I: control animals (negative control) given only placebo, Group II: (positive control) are animals orally given combination of antioxidants [vitamin C (Vit C), vitamin E (Vit E), β-carotene and sodium selenite (Se)] daily for 3 days, Group III: Rats were given only indomethacin, Group IV: animals were given of antioxidants combination for 3 days, last dose was given 2 hr before the administration of indomethacin. Group V: Animals receiving ranitidine for 3 days (second positive control). Group VI: Animals received ranitidine for 3 days, last dose was given 2 hr before to indomethacin administration. Indomethacin caused degenerative morphological and biochemical changes, which were reversed on antioxidants administration. As a result, we propose that antioxidants combination would be therapeutically beneficial for treating indomethacin-induced lesions of small intestine. PRACTICAL APPLICATIONS: Indomethacin is a widely preferred nonsteroidal anti-inflammatory drug (NSAID) but its side effects on gastrointestinal system are well known. Indomethacin also causes production of reactive oxygen species. Antioxidants and selenium has protective effects. According to the results of this study, antioxidants and selenium can be used as a food supplement for preventing NSAID-induced side effects and toxicity.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Ascorbic Acid; Humans; Indomethacin; Intestinal Diseases; Intestine, Small; Male; Oxidative Stress; Ranitidine; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Selenium

Parquetina nigrescens is a medicinal herb with recognized antioxidant properties and potential to alleviate conditions associated with oxidative stress, including gastric ulcers. We investigated the protective potential of methanol extract of Parquetina nigrescens (MEPN) against ischemia-reperfusion injury in the intestine of rats. Thirty (30) male Wistar albino rats were randomly assigned into five groups with Group I made up of control rats and Group II consisting of rats experimentally subjected to ischemia and reperfusion (IR) by clamping of the superior mesenteric artery (SMA) for 30 minutes and 45 minutes, respectively. Groups III and IV rats also had IR, but were initially pre-treated with MEPN at 500 mg/kg and 1000 mg/kg respectively, for seven days. Rats in Group V were also pre-treated with Vitamin C, for seven days, before induction of IR. The results showed marked reduction in intestinal epithelial lesions in groups treated with MEPN, compared to the IR group which had severe villi erosion, inflammatory cell infiltration and hemorrhages. There were significant increases in Malondialdehyde (MDA) and significant reductions in reduced glutathione (GSH) and Glutathione S-transferase (GST) activity with IR injury, while pre-treatment with either MEPN or Vitamin C prevented these effects. Increases in Glutathione peroxidase (GPX), Catalase (CAT) and Superoxide dismutase (SOD) with IR provided evidence for adaptive responses to oxidative injury during IR and preservation of enzyme activity by MEPN and Vitamin C. Taken together, Parquetina nigrescens provided considerable alleviation of intestinal injury produced by IR, at values much as effective as that offered by Vitamin C.

Topics: Animals; Antioxidants; Ascorbic Acid; Catalase; Cryptolepis; Disease Models, Animal; Glutathione; Glutathione Peroxidase; Glutathione Transferase; Intestinal Diseases; Male; Malondialdehyde; Methanol; Oxidative Stress; Plant Extracts; Rats; Rats, Wistar; Reactive Oxygen Species; Reperfusion Injury; Superoxide Dismutase

Pre-induction of heme oxygenase (HO)-1, which is regarded as an effective method of "organ preconditioning", exerts beneficial effects during hemorrhagic shock (HS). However, the available HO-1 inducers exhibit disadvantages such as toxicity or complex technical requirements. Therefore, a safe and convenient HO-1 inducer would be promising and could be exploited in the treatment of foreseeable hemorrhaging, such as prior to major surgery. Here we investigated the effect of vitamin C (VitC), a common antioxidant, on intestinal HO-1 expression and examined whether VitC pretreatment prevented HS related intestinal tissue injuries after HO-1 induction. First, we conducted an in vitro study and found that HO-1 expression in rat intestinal epithelial cells (IEC-6) was induced by non-toxic VitC in a time and concentration dependent manner, and the mechanism was related to the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Next, we conducted an in vivo study and found that VitC induced intestinal HO-1 protein expression (mainly observed in the intestinal epithelial cells) and HO-1 activity in normal SD rats, and that these HO-1 levels were further enhanced by VitC in a rat model of HS. The HS related intestinal injuries, including histological damage, pro-inflammatory cytokine levels (tumor necrosis factor and interleukin-6), neutrophil infiltration and apoptosis decreased after VitC pretreatment, and this alleviating of organ injuries was abrogated after the inhibition of HO-1 activity by zinc protoporphyrin-IX. It was of note that VitC did little histological damage to the intestine of the sham rats. These data suggested that VitC might be applied as a safe inducer of intestinal HO-1 and that VitC pretreatment attenuated HS related intestinal injuries via the induction of HO-1.

Topics: Animals; Antioxidants; Apoptosis; Ascorbic Acid; Cells, Cultured; Disease Models, Animal; Gene Expression Regulation; Heme Oxygenase-1; Intestinal Diseases; Intestines; MAP Kinase Signaling System; Rats; Rats, Sprague-Dawley; Shock, Hemorrhagic

Our purpose was to determine whether the administration of anti-oxidant vitamins could reduce dose-limiting toxicity from radio-immunotherapy (RAIT) and thereby allow higher escalation of RAIT doses. Lipophilic vitamins A and E were administered i.p. and hydrophilic vitamin C was administered i.m. for 14 days (3 days pre-RAIT through 11 days post-RAIT) alone or with bone marrow transplantation (BMT) to either BALB/c mice for toxicity studies or to nude mice bearing s.c. GW-39 human colonic cancer xenografts for therapy studies. The maximal tolerated dose (MTD) of RAIT ((131)I-MN14 anti-CEA IgG) that results in no lethality was determined for mice that did not receive vitamins or BMT and those that did receive one or both interventions. Body weight, peripheral white blood cell (pWBC) and platelet (PLT) counts and tumor growth were also measured. Administration of vitamins (equivalent of 3.5 IU/day vitamin A, 0.107 IU/day vitamin E and 4.0 mg/day ascorbic acid) to mice along with BMT increased the MTD by 42% and reduced body weight loss associated with RAIT. Vitamins also reduced the magnitude of RAIT-induced myelosuppression. As early as day 7 after RAIT, vitamins increased WBC counts following both a 400 microCi and a 500 microCi dose. On day 14 after the 400 microCi dose of RAIT (day 7 post-BMT), the additive effect of BMT and vitamin could be detected. Tumor growth was not adversely affected by vitamin administration.

Topics: Animals; Antioxidants; Ascorbic Acid; Body Weight; Bone Marrow Diseases; Bone Marrow Transplantation; Colonic Neoplasms; Humans; Intestinal Diseases; Leukocyte Count; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Transplantation; Platelet Count; Radioimmunotherapy; Vitamin A; Vitamin E

Topics: Adult; Ascorbic Acid; Female; Humans; Intestinal Absorption; Intestinal Diseases; Male; Middle Aged; Oxalates; Urinary Calculi

Ascorbic acid, thiamin, niacin, pyridoxine, and folic acid status was evaluated in eight physiologically stable home parenteral nutrition patients. Six of these subjects received these vitamins as a twice weekly bolus and were studied over a period of 6 days. All vitamin levels were normal except for blood thiamin which was low, 72 h after each bolus. Since transketolase levels remained normal, this fall in blood thiamin probably had no functional significance. The urine excretion pattern of niacin and pyridoxine indicated normal metabolism and retention of these vitamins. Two patients, who required only parenteral fluid and electrolytes to remain weight stable, received none of these vitamins parenterally, but also maintained adequate vitamin status. These results suggest that in long term home parenteral nutrition patients these five vitamins can safely be given twice weekly, rather than daily, and that short bowel patients who maintain their weight without intravenous calories and protein also assimilate adequate amounts of these proximally absorbed water soluble vitamins from their diet.

Topics: Adult; Aged; Ascorbic Acid; Aspartate Aminotransferases; Drug Administration Schedule; Female; Folic Acid; Humans; Intestinal Diseases; Male; Middle Aged; Niacin; Parenteral Nutrition; Parenteral Nutrition, Total; Pyridoxine; Thiamine; Transketolase; Vitamins

Topics: Anal Canal; Ascorbic Acid; Humans; Intestinal Diseases; Rectum; Vitamins