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- Thuvander, A., et al.
(author)
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Levels of ochratoxin A in blood from Norwegian and Swedish blood donors and their possible correlation with food consumption
- 2001
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In: Food and Chemical Toxicology. - 0278-6915 .- 1873-6351. ; 39:12, s. 1145-1151
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Journal article (peer-reviewed)abstract
- Blood levels of ochratoxin A were determined in 406 Scandinavian blood donors (206 from Oslo, Norway, and 200 from Visby on the island of Gotland, Sweden), using an HPLC method. In connection with the blood collection, the subjects were asked to fill in a food questionnaire to obtain individual dietary information relevant to ochratoxin A exposure. The mean plasma level of ochratoxin A was 0.18 ng/ml in Oslo and slightly higher, 0.21 ng/ml (P = 0.046) in Visby. There was no correlation between plasma levels of ochratoxin A and the estimated total dietary intake of ochratoxin A based on consumption data and levels in food (retrieved from the literature), neither was the plasma level of ochratoxin A correlated with the total amount of food consumed. However, consumption of several foods, including cereal products, wine, beer and pork, were to some minor degree related to high plasma levels of ochratoxin A. The strongest correlations (correlation coefficient r >0.4; P <0.001) were observed for women in relation to the consumption of beer or medium brown bread. Correlation analysis of combinations of two or more food categories did not result in any statistically significant correlation.
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- Petersén, Åsa, et al.
(author)
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Brain-derived neurotrophic factor inhibits apoptosis and dopamine-induced free radical production in striatal neurons but does not prevent cell death
- 2001
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In: Brain Research Bulletin. - 0361-9230. ; 56:3-4, s. 331-335
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Journal article (peer-reviewed)abstract
- In hereditary Huntington's disease, a triplet repeat disease, there is extensive loss of striatal neurons. It has been shown that brain-derived neurotrophic factor (BDNF) protects striatal neurons against a variety of insults. We confirmed that BDNF enhances survival and DARPP-32 expression in primary striatal cultures derived from postnatal mice. Furthermore, BDNF inhibited intracellular oxyradical stress triggered by dopamine, and partially blocked basal and dopamine-induced apoptosis. Nevertheless, BDNF failed to rescue striatal neurons from dopamine-induced cell death. Therefore, BDNF inhibits free radical and apoptotic pathways in medium spiny neurons, but does so downstream from the point of commitment to cell death.
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- Samsioe, Göran, et al.
(author)
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Changes in lipid and lipoprotein profile in postmenopausal women receiving low-dose combinations of 17 beta-estradiol and norethisterone acetate
- 2002
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In: Menopause. - 1530-0374. ; 9:5, s. 335-342
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Journal article (peer-reviewed)abstract
- Objective: To evaluate the modification of lipid and lipoprotein by use of low doses of continuous-combined formulations of 17beta-estradiol (E-2) and norethisterone acetate (NETA) in healthy postmenopausal women. Design: The study was designed as a double-blind, randomized, placebo-controlled trial. A total of 120 healthy postmenopausal women were randomized to one of three treatment arms: (1) placebo group (n = 40); (2) E-2/NETA 0.25-mg group-subjects receiving oral continuous-combined E-2 1 mg and NETA 0.25 mg (n = 40); (3) E2/NETA 0.5-mg group-women who were treated with E-2 1 mg and NETA 0.5 mg (n = 40). The duration of study was 12 months. Plasma levels of total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and very low-density lipoprotein (VLDL) cholesterol, triglycerides, lipoprotein(a), apolipoprotein A and apolipoprotein B were determined on four occasions (i.e., baseline, 3-, 6-, and 12-month visits). Results: There were no differences in the baseline characteristics among the three groups. A total of 102 women completed the study, resulting in a compliance rate of 85%. There was a significant reduction of total cholesterol, LDL cholesterol, and lipoprotein(a) in both combined groups when compared with placebo. The level of apolipoprotein B declined significantly only in the E-2/NETA 0.25-mg group. Decrements were observed within 3 months of treatment and maintained thereafter. No significant changes were found in triglycerides, VLDL cholesterol, HDL cholesterol, apolipoprotein A, and LDL/HDL ratio. Between the two active combined groups, no statistically significant differences were noted. Conclusion: Favorable changes in lipids and lipoproteins were associated with the low dose of E-2/NETA combinations. These effects may contribute to the reduction or prevention of atherogenesis in postmenopausal women.
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