Benzoic Acid Ethyl Ester Research Articles

3-m-bromoacetylamino benzoic acid ethyl ester: a new cancericidal agent that activates the apoptotic pathway through caspase-9

The mechanism underlying the cancericidal activity of 3-m-bromoacetylamino benzoic acid ethyl ester (3-BAABE) was investigated. 3-BAABE exerted a strong cancericidal effect on human leukemia and lymphoma cells (ic50 < 0.2 μg/mL) and on cell lines of prostate, colon, ductal, and kidney cancer (ic50 0.8 to 0.88 μg/mL). Multiple drug resistance (MDR) had no effect on the susceptibility of human lymphoma cells to 3-BAABE, since Daudi/MDR20 and wild-type Daudi cells had a similar susceptibility to the cytotoxic effect of 3-BAABE. The cancericidal effect of 3-BAABE, which was not associated with changes in the cell cycle, was mediated by apoptosis. Thus, cells exposed to 3-BAABE displayed the DNA fragmentation ladder characteristic for apoptosis, associated with a marked increase of the activity of apoptosis effector caspases-3 and -6, which was followed by proteolytic cleavage of DNA fragmentation factor (DFF) and poly(ADP-ribose) polymerase (PARP). Exposure of tumor cells to 3-BAABE increased the activity of apical caspase-9, but had no effect on caspase-8. Complete inhibition of 3-BAABE-induced apoptosis was exerted by LEHD-FMK, a caspase-9 inhibitor. DEVD-FMK, a caspase-3 inhibitor, and VEID-FMK, a caspase-6 inhibitor, partially inhibited 3-BAABE-induced apoptosis, whereas exposure to IETD-FMK, a caspase-8 inhibitor, had no effect. The fragmentation and elevated activity of caspase-9 in 3-BAABE-treated cells and the fact that only an inhibitor of caspase-9 abrogated 3-BAABE-induced apoptosis indicate that 3-BAABE is a distinctive compound that elicits apoptosis through a pathway that is limited specifically to activation of apical caspase-9.

Chlorimuron Dissipation in Water and Soil at 5 and 25 °C

Chlorimuron, 2-[[[[(4-chloro-6-methoxy-2-pyrimidinyl)amino]carbonyl]amino]sulfonyl]benzoic acid ethyl ester, was added to water (pH 7.5, hardness = 110 mg of CaCO 3 /L) and soil (sandy loam, pH 5.2) to determine the rates of dissipation at 5 and 25 °C. Radioactivity of both pyrimidine- and phenyl- 14 C-labeled chlorimuron was quantitatively recovered from water after incubation for 112 days. Greater than 85% of the radioactivity was recovered from the soil treatments after 56 days of incubation. Extractable radioactivity in the soil decreased with time. The rate of degradation of chlorimuron in water followed zero-order kinetics (R 2 > 0.95). Less than 7% of the chlorimuron degraded at 5 °C, and the slope of the zero-order constant did not differ from zero. Half-life for chlorimuron in water at 25 °C ranged from 388 to 725 days, depending upon treatment. Dissipation of chlorimuron appeared to be greater in light than dark treatments. In soil, chlorimuron dissipation was described by first-order kinetics and half-life ranged from 17 to 22 days. Probable degradation products (saccharin, ethyl benzoate sulfonamide, and pyrimidine amine) in soil and water were identified in the methanol eluate by thin layer chromatography. Ethyl benzoate sulfonamide and pyrimidine amine are hydrolysis products of chlorimuron. Less than 1% of the radioactivity from water was evolved as carbon dioxide. Three to 5% of the radioactivity was evolved as carbon dioxide from the nonsterile soil treatment. Temperature appears to be a significant factor affecting chlorimuron dissipation in soil and water. Light may also enhance chlorimuron dissipation in water.

Changes in Plasma Sex Steroids in Females of Two Sympatric Leptodactylus from Subtropical South America

Changes in Plasma Sex Steroids in Females of Two Sympatric Leptodactylus from Subtropical South America

The Effect of BAS 145138 Safener on Chlorimuron Ethyl Metabolism and Toxicity in Corn

Abstract BAS 145138 was moderately effective in protecting corn from injury due to chlorimuron ethyl. BAS 145138 increased the I50 of chlorimuron ethyl to corn, determined by root-growth in a sandy loam soil, from 6 g chlorimuron ethyl/ha to 25 g/ha. BAS 145138 caused an increase in the rate of chlorimuron ethyl metabolism , but it did not effect the rate of chlorimuron ethyl uptake or the nature of the metabolites produced. Major metabolites included chlorimuron ethyl hydroxylated in the pyrimidine ring (hydroxychlorimuron ethyl), the glucoside of hydroxychlorimuron ethyl, the glutathione conjugate formed by displacement of chlorine, a metabolite characterized as the glutathione conjugate sulfoxide or a hydroxylated glutathione conjugate, four unidentified polar metabolites, and 2-sulfonylamino benzoic acid ethyl ester. Metabolites were characterized by mass spectrometry and hydrolysis. It was concluded that BAS 145138 partially protects corn from chlorimuron ethyl by causing an increase in the rate of herbicide metabolism by hydroxylation, glucoside conjugation and by glutathione conjugation.