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111.
OBJECTIVES: This study explored correlates with and changes in the prevalence of environmental tobacco smoke (ETS) exposure of children in the home. METHODS: We used multiple logistic regression to explore ETS exposures as reported in the 1992 and 2000 National Health Interview Survey. RESULTS: ETS exposure in homes with children declined from 35.6% to 25.1% (P <.001) between 1992 and 2000, whereas smoking prevalence declined 26.5% to 23.3%. Home ETS exposures were more prevalent among non-Hispanic Whites than among African Americans (adjusted odds ratio [AOR] = 0.702; 95% confidence interval [CI] = 0.614, 0.802), Asian Americans (AOR = 0.534; 95% CI = 0.378, 0.754), and Hispanics (AOR = 0.388; 95% CI = 0.294, 0.389). Exposures declined across all groups, with greater gains in higher education and income groups. CONCLUSIONS: Home ETS exposure declined sharply between 1992 and 2000, more than would be predicted by the decline in adult smoking prevalence.  相似文献   
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The effects of increasing mitochondrial oxidative phosphorylation (OXPHOS), by enhancing electron transport chain components, were evaluated on 1-methyl-4-phenylpyridinium (MPP+) toxicity in brain neuroblastoma cells. Although glucose is a direct energy source, ultimately nicotinamide and flavin reducing equivalents fuel ATP produced through OXPHOS. The findings indicate that cell respiration/mitochondrial O(2) consumption (MOC) (in cells not treated with MPP+) is not controlled by the supply of glucose, coenzyme Q(10) (Co-Q(10)), NADH+, NAD or nicotinic acid. In contrast, MOC in whole cells is highly regulated by the supply of flavins: riboflavin, flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), where cell respiration reached up to 410% of controls. In isolated mitochondria, FAD and FMN drastically increased complex I rate of reaction (1300%) and (450%), respectively, having no effects on complex II or III. MPP+ reduced MOC in whole cells in a dose-dependent manner. In isolated mitochondria, MPP+ exerted mild inhibition at complex I, negligible effects on complexes II-III, and extensive inhibition of complex IV. Kinetic analysis of complex I revealed that MPP+ was competitive with NADH, and partially reversible by FAD and FMN. Co-Q(10) potentiated complex II ( approximately 200%), but not complex I or III. Despite positive influence of flavins and Co-Q(10) on complexes I-II function, neither protected against MPP+ toxicity, indicating inhibition of complex IV as the predominant target. The nicotinamides and glucose prevented MPP+ toxicity by fueling anaerobic glycolysis, evident by accumulation of lactate in the absence of MOC. The data also define a clear anomaly of neuroblastoma, indicating a preference for anaerobic conditions, and an adverse response to aerobic. An increase in CO(2), CO(2)/O(2) ratio, mitochondrial inhibition or O(2) deprivation was not directly toxic, but activated metabolism through glycolysis prompting depletion of glucose and starvation. In conclusion, the results of this study indicate that the mechanism of action for MPP+, involves the inhibition of complex I and and more specifically complex IV, leading to impaired OXPHOS and MOC. Moreover, flavin dervatives control the rate of complex I/cellular respiration and Co-Q10 augments complex II [corrected].  相似文献   
113.
BACKGROUND: Impaired growth accompanying thalassaemia major poses diagnostic and therapeutic problems. AIM: To test the hypothesis that impaired growth of children with thalassaemia major might be corrected, partially or totally, by increasing their caloric intake. PATIENTS AND METHODS: In a prospective controlled study, thirty selected children with thalassaemia major and 30 normal age and sex-matched controls were recruited. The dietary intake of both groups was evaluated. Nutritional status was assessed by measuring the weight, body mass index (BMI), mid-arm circumference (MAC), triceps skin fold thickness (SFT) and serum albumin and insulin-like growth factor-I (IGF-I) concentrations. The thalassaemic group was then, randomly divided into two equal groups. One group was given 8 weeks of high-caloric diet (130-150% of the caloric recommendation for age and sex) and the other was given the normal caloric requirement. RESULTS: Initially the BMI, triceps SFT and MAC of children with thalassaemia were significantly decreased compared to those for the normal control group. IGF-I and albumin concentrations of thalassemic children before nutritional supplementation (69 +/- 20.5 ng/m and 3.65 +/- 0.67 g/dl, respectively) were significantly lower than those for normal age and sex-matched children (162.5 +/- 24 ng/ml and 4.29 +/- 0.66 g/dl, respectively). After nutritional supplementation for 8 weeks the MAC, SFT and BMI, IGF-I (88.4 +/- 27.3 ng/ml) and albumin concentrations (3.85 +/- 0.85 g/dl) increased significantly (P < 0.05) in the thalassaemic children given the supplementation compared to those without supplementation, however, they were still lower than normal children. CONCLUSIONS: Increased caloric dietary intake increased significantly IGF-I levels in thalassaemic children. This was accompanied with increased BMI, mid-arm circumference and skin fold thickness. Growth impairment of children with thalassaemia major, without endocrinopathy and/or cardiomyopathy, can be partially corrected by increasing caloric intake.  相似文献   
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Acetyl-L-carnitine (ALCAR) plays an integral role in the transport of long chain fatty acids across the inner mitochondrial membrane for oxidative phosphorylation. In non-human primates, administration of ALCAR was reported to prevent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurological injury to the substantia nigra. The present study investigates the effects of ALCAR against the toxicity of 1-methyl-4-phenylpyridinium (MPP(+)), the neurotoxic metabolite of MPTP, in murine brain neuroblastoma cells. MPP(+), a potent mitochondrial toxin, induced a dose-dependent reduction in mitochondrial oxygen consumption and cell viability, corresponding to an accelerated rate of cellular glucose utilization. Treatment with ALCAR, but not L-carnitine, prevented MPP(+) toxicity and partially restored intracellular ATP concentrations, but did not reverse the MPP(+)-induced loss of mitochondrial oxygen consumption. These data indicate that protective effects are independent of oxidative phosphorylation. ALCAR had a substantial glucose sparing effect in both controls and MPP(+)-treated groups, demonstrating a potential role in enhancing glucose utilization through glycolysis. Antagonizing the entry of fatty acids into the mitochondria, with either insulin or malonyl CoA, did not interfere with ALCAR protection against MPP(+). On the contrary, insulin potentiated the protective effects of ALCAR. In conclusion, these data indicate that ALCAR protects against MPP(+) toxicity, independent of mitochondrial oxidative capacity or beta-oxidation of fatty acids. In contrast, the protective effects of ALCAR appear to involve potentiation of energy derived from glucose through anaerobic glycolysis.  相似文献   
116.
Ovarian steroid hormones, estrogen and progestin, affect the function of the serotonin neural system by inhibiting serotonin re-uptake through allosteric interaction with the serotonin transporter (SERT) in a nongenomic mechanism. Blocking or reducing serotonin re-uptake at the synapse alleviates depression. The aim of this study was to test the effect of compounds of the isoflavan and isoflavene groups, subclasses of the flavonoids family, on serotonin re-uptake and to compare the results with the effect of other known phytoestrogens like genistein and daidzein to relate the activity of these compounds to their structure. The effect of these compounds on the re-uptake of radioactive serotonin was assayed in HEK-293 cells stably expressed the recombinant human serotonin transporter (hSERT). The results demonstrated that the isoflavans glabridin and 4'-O-methylglabridin (4'-OMeG) and the isoflavene glabrene inhibited serotonin re-uptake by 60, 53 and 47%, respectively, at 50 microM, whereas resorcinol, the isoflavan 2'-O-methylglabridin (2'-OMeG), and the isoflavones genistein and daidzein were inactive. The inhibition of serotonin re-uptake is dose dependant with glabridin and estradiol. These results emphasize the importance of the lipophilic part of the isoflavans, as well as the hydroxyl at position 2' on ring B. In conclusion, this study showed that several isoflavans are unique phytoestrogens, which like estradiol, affects the serotonergic system and inhibits serotonin re-uptake and, thus, potentially may be beneficial for mild to moderate depression in pre- and postmenopausal women.  相似文献   
117.
We conducted a study in Egypt to assess the determinants of organochlorine serum levels among premenopausal women and the risk of premenopausal breast cancer for women with high organochlorine serum levels. We included 69 breast cancer patients and 53 controls consisting of visitors to the hospitals of the cancer patients. We found low levels of dichlorodiphenyldichloroethylene (DDE), total dichlorodiphenyltrichloroethane, and beta-hexacholorhexane (beta-HCH) in most subjects. Mean DDE levels were 12.7 +/- 20.3 ppb for cases and 16.6 +/- 30.1 ppb for controls (P = 0.60); beta-HCH levels were 2.1 +/- 3.8 ppb for patients and 2.1 +/- 3.9 ppb for controls (P = 0.71). Interestingly, subjects with low levels had breast fed their children for an average period of 18 months. Women with no lactation history had much higher organochlorine levels than women who breast fed (P = 0.002 for DDE). Younger age, older age at first childbirth, and shorter duration of breast feeding were significant predictors of higher levels of serum DDE levels. Younger age, older age at first childbirth, and higher body mass index were significant predictors of higher beta-HCH levels. This study suggests that organochlorine serum levels in Egyptian women are quite low, but indicates an effect of breast feeding in eliminating organochlorines, which would imply exposure to children. Organochlorine serum level was not a risk factor of breast cancer in this population.  相似文献   
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Two new flavonol glycosides from leaves of Koelreuteria paniculata   总被引:2,自引:0,他引:2  
Two new flavonol glycosides were isolated from dried leaves of Koelreuteria paniculata Laxm. (Sapindaceae) and characterized as 6,8-dihydroxy-afzelin and afzelin 3"-O-gallate, based on chemical and spectral evidences, in addition to nine known polyphenolic metabolites, including eight isolated for the first time from this species.  相似文献   
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