55-98-1Busulfan

产品属性：

Cas No.55-98-1

别名

化学名 4-methylsulfonyloxybutyl methanesulfonate

分子式 C6H14O6S2

分子量 246.3

溶解度 ≥ 12.3mg/mL in DMSO

储存条件 Store at -20°C
General tips  For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping Condition     Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述：
DNA alkylating agent is attached to the guanine base of DNA and stops tumor growth by crosslinking guanine nucleobases in DNA double-helix strands and causes DNA damage [1].

In normal human diploid WI38 fibroblasts, busulfan (7.5-120 μM) induced senescence in a dose-dependant way, which was associated with prolonged activation of c-Jun NH2-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38) and extracellular signal-regulated kinase (Erk) [2]. The induction of senescence was initiated by the transient depletion of intracellular glutathione (GSH) and then an increase in reactive oxygen species (ROS) production, which activated the Erk and p38 MAPK pathway [1].

In the adult mouse testis, busulfan induced apoptosis and decreased testis weight. In the first week, apoptosis mainly occured to spermatogonia. In the following week, spermatogonia-specific markers Stra 8 and c-kit were reduced but Gli I remained constant, which indicated apoptosis of differentiating type A spermatogonia [3].

References:

[1].  Probin V, Wang Y, Zhou D. Busulfan-induced senescence is dependent on ROS production upstream of the MAPK pathway. Free Radic Biol Med, 2007, 42(12): 1858-1865.

[2].  Probin V, Wang Y, Bai A, et al. Busulfan selectively induces cellular senescence but not apoptosis in WI38 fibroblasts via a p53-independent but extracellular signal-regulated kinase-p38 mitogen-activated protein kinase-dependent mechanism. J Pharmacol Exp Ther, 2006, 319(2): 551-560.

[3].  Choi YJ, Ok DW, Kwon DN, et al. Murine male germ cell apoptosis induced by busulfan treatment correlates with loss of c-kit-expression in a Fas/FasL- and p53-independent manner. FEBS Lett, 2004, 575(1-3): 41-51.