KKL 顾客使用本产品发表的 1 篇科研文献

L-Buthionine-(S,R)-sulfoximine is a cell-permeable, potent, fast acting and irreversible inhibitor of g-glutamylcysteine synthetase and depletes cellular glutathione levels. The IC₅₀ value of L-Buthionine-(S,R)-sulfoximine on melanoma, breast and ovarian tumor specimens are 1.9 μM, 8.6 μM, and 29 μM, respectively.

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).
L-Buthionine-(S,R)-sulfoximine (BSO) induces ferroptosis in cancer cells.

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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