The sulfhydryl borane Na[sub 2][sup 10]B[sub 12]H[sub 11]SH (BSH) was developed as a capture agent for BNCT about 20 years ago and is the compound currently used clinically in Japan for BNCT of malignant brain tumors. Tumor [sup 10]B concentrations following the infusion of the oxidized BSH, a disulfide dimer (Na[sub 4][sup 10]B[sub 24]H[sub 22]S[sub 2]), are nearly twice those obtained following administration of equal amounts of boron as BSH. Also, the rate of decrease of tumor [sup 10]B concentration is slower after dimer infusion than after BSH infusion. When BNCT was administered to rats bearing intracerebral gliosarcomas, the animals infused with dimer had a significant longer median survival time. Dimer, on the other hand, induces a moderately severe, but reversible, hepatotoxicity which may complicate its use in humans. Intracellular glutathione plays an important role in defense against radical-mediated tissue injury. Glutathione monoesters have been reported to have a protective effective on cisplatin toxicity and on radical-induced acute pancreatitis. We investigated the possibility of reducing dimer-induced hepatotoxicity by pre-administration of GSH-ME. The results indicate that not only does the pre-administration of GSH-ME markedly reduce dimer-induced hepatotoxicity, but also results in nearly a doubling of tumor boron concentration. Furthermore, GSH-ME markedly increases tumor boron uptake and retention following administration of BSH
