In vitro: Thiamine (50 mM), in addition to its nutritional value, induces systemic acquired resistance (SAR) in rice, tobacco, cucumber, and Arabidopsis. Thiamine-treated rice, Arabidopsis (Arabidopsis thaliana), and vegetable crop plants shows resistance to fungal, bacterial, and viral infections. Thiamine treatment induces the transient expression of pathogenesis-related (PR) genes in rice and other plants. In addition, Thiamine treatment potentiates stronger and more rapid PR gene expression and the up-regulation of protein kinase C activity. Vitamin B1 (10 μM) prevents acetaldehyde-induced inhibition of myocyte shortening in adult rat ventricular myocytes. Vitamin B1 (10 μM) effectively blunts the acetaldehyde-induced depression in ±dL/dt in adult rat ventricular myocytes. Vitamin B1 (10 μM) prevents acetaldehyde-induced shortening of time-to-peak shortening in adult rat ventricular myocytes. Vitamin B1 (10 μM) prevents acetaldehyde-induced elevation in both protein carbonyl formation and caspase-3 activation in adult rat ventricular myocytes. Thiamine uptake is energy- and temperature-dependent, pH-sensitive, Na+-independent, saturable at both the nanomolar (apparent Km, 30 nM) and the micromolar (apparent Km, 1.72 mM) concentration ranges in ARPE-19 cells. Uptake of Thiamine is adaptively regulated by extracellular substrate level via transcriptionally mediated mechanisms that involve both hTHTR-1 and hTHTR-2 in ARPE-19 cells, it is also regulated by an intracellular Ca2+-calmodulin-mediated pathway. Thiamine-responsive megaloblastic anemia (TRMA) fibroblasts are rescued from death with 10 nM-30 nM Thiamine (in the range of normal plasma thiamine concentrations). Normal fibroblasts exhibits saturable, high-affinity thiamine uptake (Km 400 nM-550 nM; Vmax 11 pmol/min/1×106 cells), while TRMA fibroblasts lacks detectable high-affinity uptake. At 30 nM Thiamine, the rate of uptake of Thiamine by TRMA fibroblasts is 10-fold less than that of wild-type, which explains the increased apoptosis of TRMA fibroblasts.
In vivo: Thiamine deficiency results in amyloid precursor protein immunoreactivity accumulated in swollen neurites within, or around lesions in rats, or in abnormal clusters in mice.
|Cell lines||HL-60 cells|
|Preparation method||HL-60 cells were pre-treated with 0.25 μg/ml of either cycloheximide or tetrathylammonium, a big potassium channel (BK) blocker, for 2 hours and then cultured for 12 hours with or without thiamine (100 μM) and stained with Giemsa.|
|Incubation time||12 h|
|Solubility (25°C)||68 mg/mL in water|
Powder -20°C 3 years ; 4°C 2 years
In solvent -80°C 6 months ; -20°C 1 month
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.
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