Thiamine HCl (Vitamin B1) Vitamin Produit chimique

Thiamine HCl (Vitamin B1) (50 mM), in addition to its nutritional value, induces systemic acquired resistance (SAR) in rice, tobacco, cucumber, and Arabidopsis. It also confers resistance to fungal, bacterial, and viral infections in treated rice, Arabidopsis (Arabidopsis thaliana), and vegetable crop plants. This compound induces the transient expression of pathogenesis-related (PR) genes in rice and other plants, and potentiates stronger and more rapid PR gene expression along with up-regulation of protein kinase C activity. [1] At a concentration of 10 μM, it prevents acetaldehyde-induced inhibition of myocyte shortening in adult rat ventricular myocytes, effectively blunts the acetaldehyde-induced depression in ±dL/dt, and prevents acetaldehyde-induced shortening of time-to-peak shortening. Furthermore, it inhibits acetaldehyde-induced elevation in both protein carbonyl formation and caspase-3 activation in adult rat ventricular myocytes. [2] Its uptake is energy- and temperature-dependent, pH-sensitive, Na+-independent, and 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 this compound is adaptively regulated by extracellular substrate level via transcriptionally mediated mechanisms that involve both hTHTR-1 and hTHTR-2 in ARPE-19 cells, and is also regulated by an intracellular Ca2+-calmodulin-mediated pathway. [3] Thiamine-responsive megaloblastic anemia (TRMA) fibroblasts are rescued from death with 10 nM-30 nM of it (in the range of normal plasma thiamine concentrations). Normal fibroblasts exhibit saturable, high-affinity thiamine uptake (Km 400 nM-550 nM; Vmax 11 pmol/min/1×10⁶ cells), while TRMA fibroblasts lack detectable high-affinity uptake. At 30 nM, the rate of its uptake by TRMA fibroblasts is 10-fold less than that of wild-type, which explains the increased apoptosis of TRMA fibroblasts. [4]

Thiamine HCl (Vitamin B1) deficiency results in amyloid precursor protein immunoreactivity accumulated in swollen neurites within, or around lesions in rats, or in abnormal clusters in mice. [5]