HslO ameliorates arrested ΔrecA polA cell growth and reduces DNA damage and oxidative stress responses.

Chromosome damage combined with defective recombinase activity has been widely considered to render cells inviable, owing to deficient double-strand break repair. However, temperature-sensitive recAts polA cells grow well upon induction of DNA damage and supplementation with catalase at restrictive temperatures. These treatments reduce intracellular reactive oxygen species (ROS) levels, which suggests that recAts polA cells are susceptible to ROS, but not chronic chromosome damage. Therefore, we investigated whether polA cells can tolerate a complete lack of recombinase function. We introduced a ΔrecA allele in polA cells in the presence or absence of the hslO-encoding redox molecular chaperon Hsp33 expression plasmid. Induction of the hslO gene with IPTG resulted in increased cell viability in ΔrecA polA cells with the hslO expression plasmid. ΔrecA polA cells in the absence of the hslO expression plasmid showed rich medium sensitivity with increasing ROS levels. Adding catalase to the culture medium considerably rescued growth arrest and decreased ROS. These results suggest that hslO expression manages oxidative stress to an acceptable level in cells with oxidative damage and rescues cell growth. Overall, ROS may regulate several processes, from damage response to cell division, via ROS-sensitive cell metabolism.

(+)-4-epi-alpha-bisabolol as a major sesquiterepene constituent in the leaves of two Rosa rugosa hybrids, Martin Frobisher and Vanguard.

During an investigation of the sesquiterpene phases and contents in leaves of several Rosa rugosa hybrids (hybrid rugosas), Martin Frobisher and Vanguard were found to accumulate a large amount of (+)-4-epi-alphabisabolol (1) as a single constituent. Although glandular trichomes of Martin Frobisher on the leaves are dense, this R. rugosa hybrid produces none of the carota-1,4dienaldehyde (2) or bisaborosaol A (3) that are both found as representative sesquiterpenes of the carotane and bisabolane classes, respectively, in a glandular trichome exudate of wild-type R. rugosa. Compound 1 was also apparent as a nearly single constituent detectable by GC in the leaf constituents of Vanguard possesses sparse glandular trichomes on the leaf. Martin Frobisher and Vanguard had likely lost their capability to form carotane-type sesquiterpenes and had also lost their activity to oxygenate the C-7 allyl methyl carbon of compound 1 to convert 3. The presence of (+)-4-epi-alphabisabolol-accumulating R. rugosa hybrids is significant when considering the sesquiterpene biogenesis of Rosa rugosa.

Distribution of selenium and molybdenum and cancer mortality in Niigata, Japan.

Selenium and molybdenum have inhibitory effects on gastrointestinal carcinogenesis. We investigated the levels of selenium and molybdenum in sediments and mortality from cancers at specific sites in 19 areas of Niigata Prefecture, Japan, and compared these factors. The average concentrations of selenium and molybdenum were 0.44 +/- 0.19 ppm (micrograms/g dry weight; mean +/- standard deviation) and 3.82 +/- 1.03 ppm, respectively. Selenium was not associated significantly with cancer mortality. There were inverse correlations between molybdenum levels and female mortality from cancers of the esophagus (r = -.446, .05 < p < .1) and rectum (r = -.529, p < .05). Molybdenum was correlated positively with female mortality from cancer of the pancreas (r = .603, p < .01). Further investigations are needed for causal interpretation of these results.

Mechanism of intragastric tetramethylammonium protection against 40% ethanol injury in rat stomach.

The effect of tetramethylammonium (TMA), a ganglionic stimulant, on gastric mucosal injury induced by 40% ethanol was examined. In studies I-III, rats were treated with intragastric vehicle or TMA (1 or 10 mg/kg). In study I, 1 hr after the treatment, 40% ethanol was given intragastrically. The length of the linear corpus mucosal lesions was measured unbiasedly with a caliper after another hour. In study II, mean blood pressure was assessed before and after the treatment. In study III, 1 hr after the treatment, gastric mucus and juice volumes, and titratable acid were measured. In study IV, 40% ethanol (10 ml/kg) was administered intragastrically immediately after 0.2 or 1.4 ml of intragastric vehicle treatment. One hour later, gastric lesions score was assessed as in study I. Results show that (1) intragastric TMA dose-dependently protected against 40% ethanol-induced gastric injury; (2) neither dose of intragastric TMA increased mean blood pressure; (3) there was a dose-related increase in gastric mucus secretion for TMA 1 and 10 mg/kg, and a significant increase in gastric juice volume only for TMA 10 mg/kg; and (4) the rats treated with 1.4 ml of vehicle plus 40% ethanol had significantly less injury than those treated with 0.2 ml of vehicle plus 40% ethanol. We conclude that the protective effect of intragastric TMA can be explained by its dose-related effect in enhancing gastric mucus secretion for TMA 1 and 10 mg/kg and the significantly greater increase in gastric juice volume for TMA 10 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Involvement of alpha 2-adrenoceptors in mechanism of intragastric nicotine protection against ethanol injury in rat stomach.

To elucidate the role of alpha- and beta-adrenoceptors in the mechanism of intragastric nicotine protection against ethanol-induced gastric mucosal injury, the following studies were performed. At 0.5-hr prior to the injury study, rats were pretreated with: subcutaneous control, prazosin (0.5 mg/kg) or yohimbine (5 mg/kg) to block alpha 1- or alpha 2-adrenoceptors; or intraperitoneal control, metoprolol (2 mg/kg) or butoxamine (4 mg/kg) to block beta 1- or beta 2-adrenoceptors, respectively. At 1-hr intervals, rats received intragastric vehicle or nicotine (4 mg/kg) and 40% ethanol (10 ml/kg). Total lengths of the linear gastric corpus mucosal lesions were measured by an unbiased observer using a caliper. In a separate study, 0.5-hr after subcutaneous control or yohimbine (5 mg/kg), rats were treated with intragastric vehicle or nicotine (4 mg/kg). One hour later, gastric mucus volume, gastric juice volume and pH, and titratable acid in the gastric juice were measured. In the rat stomach, the intragastric nicotine protection against 40% ethanol-induced mucosal injury was not blocked by selective alpha 1-(prazosin), beta 1-(metoprolol), or beta 2-(butoxamine) adrenoceptor antagonists. The protection was significantly reduced although not completely abolished by selective alpha 2-(yohimbine) adrenoceptor antagonist. Yohimbine also significantly reduced basal and nicotine-stimulated increase in gastric mucus volume. These data suggest that alpha 2-adrenoceptors are involved in the protective effect of intragastric nicotine against 40% ethanol-induced gastric mucosal injury possibly by a mucus-dependent mechanism.