No abstract

Twenty-two healthy teetotal volunteers underwent gastroscopy during which biopsy samples from the antrum and body were taken for chemiluminescence assay, routine histology, and for malonyldialdehyde, xanthine oxidase and glutathione determination. Subjects were divided into 2 groups which, in a double-blind fashion, were randomly and orally given either (a) Bionormalizer 9 g at bedtime and 3 h prior examination, or (b) flavored sugar 9 g as placebo. During the second gastroscopy 40 ml of 80% ethanol were sprayed perendoscopically. Gastroscopy with biopsy was repeated 60 min later. As compared to the placebo group, subjects given Bionormalizer showed significantly reduced gastric mucosal damage at endoscopy and the histological level. When considering the placebo group, ethanol administration brought about a significant increase in the luminol-amplified chemiluminescence response in gastric mucosa as compared to the baseline value which was correlated with the histological score. The mean chemiluminescence value in the Bionormalizer group was significantly lower than in the placebo group. Ethanol ingestion brought about a significant increase in xanthine oxidase and malonyldialdehyde together with a decreased glutathione concentration. Bionormalizer significantly prevented such changes. The present data suggest that the natural antioxidant Bionormalizer when given orally promotes an effective protection against ethanol-induced gastric mucosal damage.

I The plasma availability of prednisolone after oral doses of prednisolone and its precursor, prednisone, were compared in ten normal controls and twenty-five patients with chronic active hepatitis by estimation of the area under the plasma concentration-time curve for the drug (AUC). 2 In controls, values for AUC were significantly more variable after prednisone than prednisolone, and two subjects showed markedly inefficient conversion of prednisone to prednisolone. In patients, variability was similarly wide after both preparations, but overall bioavailability after both prednisone and prednisolone was similar to that found in controls, although three patients showed subnormal values after both preparations, possibly as a result of impaired intestinal absorption. 3 Patients with biochemical and histological evidence of active hepatocellular necrosis showed evidence of impaired activation of prednisone, but this was compensated for by a decreased rate of elimination of prednisolone from the plasma. 4 It is concluded that plasma prednisolone levels will be more predictable after prednisolone than after prednisone in subjects without hepatic dysfunction. In the presence of liver disease, because of the marked variability in plasma prednisolone levels after either drug, estimation of these could be of value in those patients whose disease cannot be controlled by normal maintenance doses.

The aim of this study was to test K-17.22, an herbal formula which has been preliminarly shown to yield a significant transaminases decrease in HCV patients, in CCl4-induced liver toxicity. Wistar rats were allocated into 3 groups: A) given a 3_¢_ injection of 0

1. The degree of liver damage observed 48 h after administration of 14C ring-labelled paracetamol (3-23 mmol/kg) to rats was proportional to the amount of a highly reactive metabolite retained in the liver, bound covalently to hepatocellular proteins. 2. With increasing doses of paracetamol, urinary excretion of the glucuronide and sulphate conjugates reached a plateau, whereas the output of cysteine and mercapturic acid conjugates increased markedly. 3. The degree of covalent binding at 48 h was proportional to the rate of urinary elimination of these two latter conjugates in the first 24 h after dosing.