The results support the important role of SOD and GPx in the protective effects of OOP against organ damage induced by fecal peritonitis in rats.

This research was performed in order to determine the potential protective effects of ozonized sunflower oil (OSO) in the injury of rat gastric mucosa induced by absolute ethanol and as well as to elucidate the role of reactive oxygen species (ROS), lipid peroxidation, and some important constituents of antioxidant defense such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in these effects. OSO was administered to rats intragastrically by a cannula and it was applied during four days to animals. The doses of OSO administered daily to each group of rats were 4, 12, and 24 mg/kg, respectively, and one hour after the last treatment, absolute ethanol (1 mL/200 mg body weight) was administered. Our results showed that gastric ulcer index was significantly reduced in rats pretreated with OSO as compared with ethanol-treated controls. However, in rats pretreated with OSO, no significant reduction of TBARS content in gastric mucosa was found as compared to those rats treated with ethanol alone. In contrast, SOD and GSH-Px activities were significantly increased in gastric mucosa of OSO-pretreated rats with respect to those treated with ethanol alone. In summary, our results demonstrate that OSO pretreatment exerts protective effects in ethanol-induced gastric ulcers in rats. Furthermore, these results provide evidence that these protective effects of OSO are mediated at least partially by stimulation of some important antioxidant enzymes such as SOD and GSH-Px, which are scavengers of ROS and therefore prevent gastric injury induced by them.

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In vitro studies of lactose hydrolysis in milk with 20-125 neutral lactase units (NLUs) carried out at 38.0 degrees C for 15 min with a beta-galactosidase derived from Kluyveromyces lactis (Lactaid, Lactaid Inc, Pleasantville, NJ) resulted in 85-95% of the hydrolysis observed with standard incubation conditions (24 h at 4-5 degrees C with 1000 NLU/L). Thirty-three lactose-maldigesting Guatemalan subjects, 16 children and 17 adults, were challenged with oral doses of lactose in milk (children aged less than 12 mo, 2 g/kg body wt; children aged 12-24 mo, 15 g/kg body wt; older children and adults, 18 g/kg body wt) preincubated for 20 min at 38 +/- 0.5 degrees C with 50-125 NLU Lactaid. Under these conditions the subjects consumed milk without presenting any signs of intolerance. Furthermore, their breath-hydrogen excretion showed a 91-93% reduction when compared with a similar load of milk containing nonhydrolyzed lactose.

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