Helicobacter pylori profile in asymptomatic farmers and non-farmers.

There is a positive correlation between Helicobacter pylori infection and chronic active gastritis, peptic ulcer and gastric cancer and maltoma. There is little information on H. pylori profiles in farmers and non-farmers in the literature. Our main objective was to study the H. pylori profiles in farmers and non-formers in the United Arab Emirates. A prospective study of 151 subjects - 76 farmers and 75 non-farmers - was undertaken by determining their IgG and IgA H. pylori antibody profiles in their serum samples. Data on lifestyle were obtained from them. Eligible subjects were those who had engaged in farming for at least five years and who had not received an anti-H. pylori treatment during the six months prior to admission into the study. Most of the farmers lived in less modern accommodation, were less educated, ate their vegetable products unwashed, did not have drinking water facilities, when compared to non-farmers. Helicobacter pylori serology by IgG and IgA was positive in 112 and 77 subjects respectively (p < 0.0001). The sensitivity values for IgG and IgA serology tests were 74.2 and 51.0% respectively (p < 0.001). There were 59 and 42 H. pylori-positive farmers by IgG and IgA H. pylori serology tests respectively (p < 0.001). Among the non-farmers, the corresponding figures were 53 and 25 (p < 0.01), and neither IgG nor IgA (p = 0.4), respectively. The H. pylori serology test was able to differentiate between farmers and non-farmers. When the discordant values between IgG and IgA tests were computed for each group of subjects, the difference was significant for both farmers and non-farmers (p < 0.001 in each case). There was no difference between the farmers and non-farmers in respect of their H. pylori profiles. The farmers have a lower standard of living than non-farmers.

Hepatoprotection of D-galactosamine-induced toxicity in mice by purified fractions from Garcinia kola seeds.

The hepatoprotective effect of a biflavonoid complex, kolaviron, and its fractions from Garcinia kola seeds, together with the possible mechanisms involved was investigated in mice intoxicated with a single dose of D-galactosamine (GalNH(2)). Likewise, the ability of vitamin E to attenuate the toxicity was examined. Kolaviron, was separated by thin-layer chromatographic technique into three fractions; Fraction I, Fraction II and Fraction III with RF values of 0.48, 0.71 and 0.76, respectively. Pretreatment with kolaviron, fraction I and fraction II at a dose of 100 mg/kg for seven consecutive days before challenge with a single dose of GalNH(2) (800 mg/ kg) significantly (P<0.05) decreased serum alanine (ALT) and aspartate (AST) aminotransferases by 67%, 70%, 71% and 39%, 35%, 46%, respectively over GalNH(2)-only intoxicated mice. Vitamin E elicited respectively 65% and 39% reduction in the GalNH(2)-induced increase in the activities of these enzymes. In addition, pretreatment with kolaviron and fraction II significantly (P<0.05) decreased the activity of microsomal gamma-glutamyl transferase (gamma-GT) by 42% and 46%, respectively. Administration of kolaviron to GalNH(2)-intoxicated mice also restored glucose-6-phosphatase to level that was comparable to the control (P<0.05). These extracts except fraction III prevented the accumulation of serum and microsomal lipid peroxidation products, and also prevented the depletion of reduced glutathione (GSH) levels in the liver of GalNH(2)-intoxicated mice. Kolaviron, fraction I and fraction II at a dose of 100 mg/kg caused an induction of glutathione-S-transferase (GSH transferase) and uridyl glucuronosyl transferase (UDPGT) activities by 31%, 34%, 35% and 29%, 65%, 56%, respectively. GalNH(2)-induced toxicity was essentially prevented as indicated by a liver histopathologic study of liver slices from mice pretreated with kolaviron, fraction I and fraction II. This study shows that treatment with kolaviron, fraction I and fraction II (purified fractions from Garcinia kola) appeared to enhance the recovery from GalNH(2)-induced hepatotoxicity, and that the fractions I and II may therefore be responsible for the observed antihepatotoxic effect of kolaviron. This protection may be due to the ability of these extracts to induce the expression of phase II drug metabolizing enzymes.

Mechanisms of action of leptin in preventing gastric ulcer.

AIM: To investigate the effects of leptin (1-20 microg/kg) on acidified ethanol (AE)- and indomethacin (Indo)-induced gastric lesions in rats and compare it with ranitidine, lanso-prazole, and omeprazole and to determine its mechanisms of actions. METHODS: Gastric ulcers, which were approximately 1 mm in width, formed in the glandular portion of the gastric mucosa produced by oral administration of either AE or Indo were taken as ulcer index. The inhibitory effect of subcutaneous administration of leptin, two proton pump inhibitors (PPIs) lansoprazole and omeprazole, or H(2)-receptor antagonist ranitidine 30 min before AE or Indo was evaluated. A radioimmunoassay was used to determine the PGE(2) concentration in the homogenate of the glandular portion of the stomach. We performed histological study of the glandular stomach for the evaluation of total, acidic, and sulfated mucus content. RESULTS: Subcutaneous administration of leptin, two PPIs lansoprazole and omeprazole or H(2)-receptor antagonist ranitidine 30 min before AE or Indo produced a dose-dependent and reproducible inhibition of gastric ulcers (GUs). This inhibition was found to be more potent than other antagonists used. In N(G)-nitro L-arginine methyl ester (L-NAME)-pretreated animals, the ulcer prevention ability of leptin in AE-induced ulcer was significantly reduced, compared to rats without L-NAME pretreatment. However, the ulcer prevention ability of leptin was not altered by L-NAME treatment in Indo-induced ulcers. Leptin produced a dose-dependent increase in PGE(2) level in the gastric glandular tissues. Leptin also increased mucus secretion. CONCLUSION: The results of the present study show that leptin inhibits GU formation by AE or Indo in a dose-dependent and reproducible manner in rats. The results also suggest that leptin prevents ulcer formation by increasing the activities of the cyclo-oxygenase and/or nitric oxide pathways and by increasing mucus secretion.