摘要:

AbstractOne of the main methods for eliminating ice‐nucleation‐active (INA+) bacteria, the micro‐organisms responsible for frost injuries to plants at mild freezing temperatures, is the use, as competitors, of other naturally occurring non‐nucleating strains (non‐INA). In the present article we investigated the cytogenetic effects of a naturally occurring non‐INA strain ofPseudomonas fluorescens(MS 1640 R3), evaluating the induction of chromosomal aberrations and sister chromatid exchanges (SCEs) in Chinese hamster ovary (CHO) cells in the absence and presence of rat S9 metabolism. The results obtained did not show any increase in either chromosomal aberrations or SCEs, both in the absence and presence of rat S9 metabolism when used as (i) intact bacteria cells, (ii) sonicated bacteria (i.e., potential endotoxins), or (iii) metabolic bacterial products (i.e., potential exotoxins) released in the growth medium. © 1995 Wil

ISSN:0270-3211    

DOI:10.1002/tcm.1770150302

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractThe effect of WR‐2721 against cyclophosphamide‐induced clastogenicity was studied using the in vivo micronucleus assay. The frequency of micronuclei in polychromatic erythrocytes in the peripheral blood of mice treated with WR‐2721 and cyclophosphamide (CP), each of the compounds at a dose of 200 mg/kg body weight, was evaluated during the 15‐day period. The suppressing effect of WR‐2721, given 30 min prior to cyclophosphamide administration, on micronuclei induced by the alkylating agent was demonstrated. The number of micronuclei was increased on day 1 after CP application and declined thereafter with the frequency of micronucleated polychromatic erythrocytes remaining lower in WR‐2721 pre‐treated mice. The modulatory effect of WR‐2721 on the clastogenic activity of cyclophosphamide in the erythropoietic system by the mouse micronucleus test was shown. © 1995

ISSN:0270-3211    

DOI:10.1002/tcm.1770150303

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractEarlier investigations from our laboratory demonstrated that human term placental peroxidase (HTPP) is capable of metabolism of xenobiotics and endogenous compounds. In this study, purified HTPP was found to bioactivate 2‐aminofluorene (2‐AF) in the presence of H2O2. 2‐AF oxidation was studied spectrophotometrically while radiometry was employed to assess the bioactivation. The rate of oxidation and covalent binding to protein and DNA was dependent upon the pH of the reaction medium and the concentration of 2‐AF, the enzyme, and H2O2. To observe maximal enzyme velocity of oxidation, the presence of 16.5 μM H2O2, 100 μM 2‐AF, 37 γg of the enzyme protein/ml, and pH 7.2 was required. Under optimal assay conditions, the range of specific activity between 130 and 165 nmol of 2‐AF oxidized/min/mg HTPP was observed. Using similar assay conditions, the magnitude of covalent binding of [3H]‐2‐AF to protein (BSA) and calf thymus DNA was found to be about 508 pmol bound/min/mg HTPP/mg BSA and 84 pmol bound/min/mg HTPP/mg DNA, respectively. Potassium cyanide and sodium azide, the known inhibitors of different peroxidases, significantly blocked both the oxidation and covalent binding of 2‐AF in a dose dependent manner. These results strongly suggest that peroxidase may be one of the important pathways responsible for the bioactivation of arylamines in human term placenta. ©

ISSN:0270-3211    

DOI:10.1002/tcm.1770150304

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractThis paper evaluates the potential effects of arecanut (Areca catechu, L.), an important ingredient of betel quid, on the garlic (Allium sativum, L.)‐modulated activities of hepatic detoxication system enzymes, acid soluble sulfhydryl content, and lipid peroxidation in mice. Mice were fed on either a normal diet or a diet containing 0.25%, 0.5%, or 1% (w/w) arecanut for 45 days. During the last 10 days of treatment oral administration of garlic at the dose level of 20 or 100 mg/kg body weight/day was supplemented. Significant modulation in the activities of phase I and phase II enzymes, –SH content, and malondialdehyde (MDA) level by garlic was observed. Garlic‐modulated alterations in glutathione S‐transferase (GST) activity and –SH content were decreased, while cytochrome b5, cytochrome P‐450, and MDA levels were further augmented by the arecanut plus garlic treatments. © 1995 Wil

ISSN:0270-3211    

DOI:10.1002/tcm.1770150305

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractThe modulatory influence of arecanut, a masticatory in several human populations, on the levels of biotransformation system enzymes in mouse liver has been studied. Swiss albino mice of either sex (4 weeks old) were fed on diets containing 0.25%, 0.5%, or 1% arecanut (w/w) for 5 weeks. In addition, a group of mice received a 1% arecanut diet for 36 weeks. The findings revealed a significant increase in hepatic levels of cytochrome b5, cytochrome P‐450, malondialdehyde (MDA), and glutathione S‐transferase (GST). The hepatic –SH content was depressed by 0.5% and 1% arecanut diets. Long‐term feeding of a 1% arecanut diet elicited changes similar to those seen following treatment for 5 weeks. Arecanut‐modulated profiles of biotransformation enzymes and antioxidant levels are suggestive of its influence in the process of carcinogenesis induced by bioactivated electrophilic species of potential chemical carcinogens among habitual arecanut chewers. Arecanut was also tested for its potency either to induce or to alter 7,12‐dimethylbenz[a]anthracene (DMBA)‐induced papillomagenesis in the skin of the mouse. Animals put on a 1% arecanut diet and treated with a standard two‐stage protocol for tumor induction developed a 5.41 tumor burden (control value: 5.76) along with 100% incidence of mice bearing papillomas (control value: 94.4%), thus signifying that dietary intake of 1% arecanut for 18 weeks could not induce/alter the mouse skin tumorigenesis pattern. © 1995

ISSN:0270-3211    

DOI:10.1002/tcm.1770150306

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractTo determine the effect of maternal diabetes and alcohol intake, separately and in combination, on fetal growth and development, pregnant rats were divided into four groups: diabetic (D), diabetic plus alcohol (DA), control (C), and control plus alcohol (CA). Diabetes was induced by administration of streptozotocin before mating and alcohol was administered by gavage (2 g/kg body weight/day) on days 6‐‐11 of gestation. Both diabetic groups (D and DA) had significantly lower weight gain during pregnancy compared to the controls (C and CA), despite the fact that the former consumed more food and water. Alcohol treatment resulted in reduced water and food intake and lower weight gain in the diabetic rats (DA), but not in the non‐diabetic rats (CA), compared to their respective controls (D and C). On day 21 of gestation fetal body weights were significantly less and placental weights were significantly greater in the diabetic groups (D and DA) compared with the non‐diabetic groups (C and CA). Differences in fetal and placental weights between rats exposed and not exposed to alcohol (C vs. CA and D vs. DA) were not significant. The number of fetuses with external malformations was significantly greater in the litters of alcohol exposed diabetic (DA) than non‐alcohol exposed (D) animals. No external or skeletal malformations were observed in fetuses of non‐diabetic rats regardless of whether or not they received alcohol (C or CA). The skeletal development of fetuses of diabetic rats, judged by the number and size of ossification centers on day 21 of gestation, was retarded when compared with fetuses of non‐diabetic rats. Alcohol further retarded skeletal development of fetuses of diabetic animals (DA vs. D), but not of fetuses of non‐diabetic rats (CA vs. C). It is concluded that maternal alcohol administration potentiates the effects of maternal diabetes on the incidence of fetal malformations and the retardation of skeletal development. © 1995

ISSN:0270-3211    

DOI:10.1002/tcm.1770150307

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

ISSN:0270-3211    

DOI:10.1002/tcm.1770150301

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY