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PubMed1990

[Vitamin B1 content of liver, brain and muscles of pregnant and nonpregnant rats with different vitamin B1 supplies].

The purpose of this publication was to examine the effects of a wide variation of dietary vitamin B1 supply (0-12,000 mg vitamin B1 per kg diet) to gravid and non gravid rats on their vitamin B1 content in liver, brain and muscle. The experiment was designed with 176 (2 x 11 x 8) female Sprague-Dawley-rats. Additionally, the organs and tissues were tested as criteria for requirement recommendations. The animals were sacrificed on the 20th day of gravidity of the pregnant rats. Before gravidity the vitamin-B1-contents were 4.7 micrograms/g liver, 2.5 micrograms/g brain and 1.5 micrograms/g muscle. At the end of the experiment the gravid rats had a 19 per cent higher liver content than the non gravids. With a dietary supply of 8-10 ppm vitamin B1 the liver content plateaued until about 120 ppm. Vitamin B1 concentration in brain was about 2 micrograms/g and gravidity was of no effect. Vitamin B1 concentration in muscle was significantly influenced by both factors and saturation was reached at 1.3 and 1.7 micrograms/g muscle. These data showed that the response of the liver to dietary supply was the most sensitive and should therefore be considered in requirements. The requirement for non gravid animals is therefore 4 mg vitamin B1 per kg diet at minimum, gravid animals should be supplied by 7 mg per kg diet.

Animals↗
PubMed2004

Acetaldehyde-induced cardiac contractile dysfunction may be alleviated by vitamin B1 but not by vitamins B6 or B12.

AIMS: Chronic alcohol exposure leads to a deficiency of group B vitamins and increased risk of alcoholic cardiomyopathy characterized by impaired ventricular contractility. This study was designed to examine the effect of group B vitamin supplementation on short-term exposure of the main alcohol metabolite acetaldehyde (ACA)-induced cardiac contractile dysfunction in rat ventricular myocytes. METHODS: Mechanical contractile properties were evaluated by an IonOptix SoftEdge system. Protein damage and apoptosis were determined by protein carbonyl and caspase-3 assays, respectively. RESULTS: Short-term (4-6 h) culture of myocytes with ACA (10 microM) depressed peak shortening amplitude, maximal velocity of shortening/relengthening, shortened duration of shortening but not the duration of relengthening. ACA exposure also enhanced protein carbonyl formation and apoptosis in ventricular myocytes. The toxin-induced mechanical defects, protein damage and apoptosis were ablated by vitamin B1 (10 microM), an essential vitamin required for DNA synthesis and repair. Vitamin B6 (10 microM) attenuated ACA-induced impairment of shortening duration. Vitamin B12 (1 mM) attenuated ACA-induced reduction in maximal velocity of shortening/relengthening. Unlike vitamin B1, none of the other ACA-elicited alterations in myocyte mechanical function were affected by vitamin B6 or vitamin B12. Vitamin B6 and vitamin B12 partially, but significantly, attenuated the ACA-induced carbonyl formation without affecting ACA-induced apoptosis. CONCLUSIONS: These data provide evidence that vitamin B1 supplementation may be protective for ACA-induced cytotoxicity through protection against protein damage and apoptotic cell death in ventricular myocytes.

Acetaldehyde↗