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L-Buthionine-(S,R)-sulfoximine
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L-Buthionine-(S,R)-sulfoximine
CAS No. : 83730-53-4
MCE 站:L-Buthionine-(S,R)-sulfoximine
产品活性:L-Buthionine-(S,R)-sulfoximine 是一种具有细胞渗透性的、有效的、快速起效的、不可逆的 G-谷氨酸半胱氨酸合成酶 (γ-glutamylcysteine synthetase) 抑制剂,可降低细胞内谷胱甘肽的水平,其对黑色素瘤、乳腺卵巢癌标本的 IC50 值分别为1.9 μM、8.6 μM 和29 μM。
研究领域:Apoptosis
作用靶点:Ferroptosis
In Vitro: L-Buthionine-(S,R)-sulfoximine (BSO: 50 μM) treatment for 48 hr results in a 95% decrease in ZAZ and M14 melanoma cell line GSH levels, and a 60% decrease in GST enzyme activity. GST-π protein and mRNA levels are significantly reduced in both cell lines. L-Buthionine-(S,R)-sulfoximine (BSO) induces oxidative stress in a cell by irreversibly inhibiting g-glutamylcysteine synthetase, an essential enzyme for the synthesis of glutathione (GSH).
In Vivo: The average number of eye-spots (mean±SEM) is 5.36±0.29 (n=46), 7.79±0.45 (n=34) and 8.78±0.61 (n=32) in untreated controls, 2 mM L-Buthionine-(S,R)-sulfoximine (BSO) and 20 mM BSO treated mice, respectively. The 2 mM BSO treatment results in ~30% more eye-spots, and the 20 mM treatment results in 40% more eye-spots compared with untreated mice. It is showed that BSO causes an elevated frequency of DNA deletions during mouse development. BSO treatment reduced GSH concentration in mouse fetuses by 55% and 70% at 2 mM and 20 mM BSO doses, respectively, compared to untreated mice. Co-treatment with 2 mM BSO and 20 mM NAC depleted GSH to a similar extent as 2 mM BSO, consistent with the function of BSO to inhibit the g-GCS enzyme indispensable for GSH synthesis. Like GSH, cysteine levels dropped following BSO treatment.
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