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PubMed1985

Modulation by taurine of the toxicity of taumustine, a compound with antitumor activity.

The antitumor activity of 2-[bis-(2-chloroethyl)-amino]ethanesulfonic acid (also referred to here as "taurine mustard" or "taumustine") was evaluated in the murine P388 and L1210 lymphocytic leukemias and in the pigmented and nonpigmented B16 melanoma systems. Treatment with a single ip dose of taumustine (40 mg/kg) resulted in a 130% increase in life-span for mice bearing P388 (intraperitoneal), a 93% increase for mice bearing L1210 (intraperitoneal), and an approximately 80% increase for mice bearing B16 melanoma (intraperitoneal). Repeated low doses (10 mg/kg) of taumustine promoted a 250% increase in life-span for mice bearing P388 (intraperitoneal), the absence of ascitic fluid from day 4 onward, and the presence of pulmonary emboli from day 5 onward. The inclusion of taurine (5 mM) in the culture medium of P388 cells in primary culture for 45 hours did not alter the cytotoxicity of taumustine, and pretreatment of the tumor-bearing host with taurine (250 mg/kg) in daily treatments with taumustine for up to 8 days did not interfere with antitumor activity (140-160% increased life-span). However, treatment of tumor-bearing mice with taurine abrogated neurotoxicity, intestinal necrosis, pulmonary emboli formation, and tail vein necrosis due to the administration of taumustine. The modulation by taurine of taumustine activity suggests that the combination of these agents offers an advantage of selectivity and host protection during chemotherapy.

Animals↗
PubMed2004

Reactions of sulphur mustard on impregnated carbons.

Activated carbon of surface area 1100 m2/gm is impregnated with 4% sodium hydroxide plus 3% Cr(VI) as CrO3 with and without 5% ethylene diamine (EDA), 4% magnesium nitrate and 5% ruthenium chloride by using their aqueous solutions. These carbons are characterized for surface area analysis by BET conventional method and exposed to the vapours of sulphur mustard (HD) at room temperature (30 degrees C). After 24 h, the reaction products are extracted in dichloromethane and analyzed using gas chromatography and mass spectrometry (GC-MS). Hemisulphur mustard, thiodiglycol, 1,4-oxathiane are observed to be the products of reaction between sulphur mustard and NaOH/CrO3/C system, whereas on NaOH/CrO3/EDA/C system HD reacted to give 1,4-thiazane. On Mg(NO3)2/C system it gave hemisulphur mustard and thiodiglycol. On RuCl3/C system it degraded to divinyl sulphone. Residual sulphur mustard is observed along with reaction products in all systems studied. Reaction mechanisms are also proposed for these interesting surface reactions. Above-mentioned carbons can be used in filtration systems for protection against hazardous gases such as sulphur mustard.

Adsorption↗
PubMed2000

Role of poly(ADP-ribose) polymerase (PARP) in DNA repair in sulfur mustard-exposed normal human epidermal keratinocytes (NHEK).

We previously reported that, in normal human epidermal keratinocytes (NHEK) cultures exposed to the alkylating compound sulfur mustard (bis-(2-chloroethyl) sulfide, HD, 0.3-1 mM), there is a rapid (< or =1 h) activation (100% above unexposed control) of the DNA repair enzyme DNA ligase I (130 kD) followed by a first-order decay (1-5 h). The DNA ligase activation is accompanied by a time-dependent (0.5-4 h) and significant DNA repair. Inhibition of another putative DNA repair enzyme, poly(ADP-ribose) polymerase (PARP), by using 3-amino benzamide does not affect DNA ligase activation following HD exposure, but increases the half-life of the activated enzyme threefold. To examine the role of PARP in HD-induced DNA ligase activation and subsequent DNA repair, we conducted studies using cultured keratinocytes in which the level of PARP had been selectively lowered (> or =85%) by the use of induced expression of antisense RNA. In these cells, there was no stimulation of DNA ligase up to 3 h, and a small stimulation (ca. 30% above unexposed control at 5-6 h after HD exposure. A time-course (0.5-6 h) study of DNA repair in HD-exposed PARP-deficient keratinocytes revealed a much slower rate of repair compared with HD-exposed NHEK. The results suggest an active role of PARP in DNA ligase activation and DNA repair in mammalian cells, and also indicate that modulation of PARP-mediated mechanisms may provide a useful approach in preventing HD toxicity.

Cell Culture Techniques↗