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D Sparling

Publications and source records attributed to D Sparling.

9 recordsLinked to original sources
PubMed2003

Aqueous-phase disappearance of atrazine, metolachlor, and chlorpyrifos in laboratory aquaria and outdoor macrocosms.

Dissipation processes are described for a combination of commonly used pesticides-atrazine (6-chloro-4-ethylamino-6-isopropylamino- s-triazine), metolachlor (2-chloro- N-[2-ethyl-6-methyl-phenyl]- N-[2-methoxy-1-methylethyl] acetamide), and chlorpyrifos ( O-O diethyl O-[3,5,6-trichloro-2-pyridinyl] phosphorothioate)-in a laboratory and outdoor pond systems. Dosing rates and timing were designed to duplicate those common in the mid-Atlantic Coastal Plain, USA. Treatments ranged from 2 and 2.5 mg/L to 0.2 and 0.25 mg/L respectively for atrazine and metolachlor, and chlorpyrifos was added at 1.0 and 0.1 mg/L in the aquaria and at 0.1 mg/L in the outdoor macrocosms. Chlorpyrifos disappearance was rapid in all of the systems and followed a two-phase sequence. Initial half-lives varied from 0.16 day to 0.38 day and showed similar rates in the aquaria and the outdoor systems. The second phase of the chlorpyrifis loss pattern was slower (18-20 days) in all the treatments except for the low herbicide treatment in the outdoor test, where it was 3.4 days. Compared to the outdoor system, herbicide losses were much slower in the aquaria, e.g., 150 days for atrazine and 55 days for metolachlor, and no appreciable loss of herbicide was apparent in the high-treated aquaria. In the outdoor systems, the half-lives for the low herbicide treatment were 27 days and 12 days, respectively, for atrazine and metolachlor, and 48 and 20 days, respectively for the high herbicide-treated pond. Very low levels of CIAT (6-amino-2-chloro-4-iso-propylamino- s-triazine) and CEAT (2-chloro-4-ethylamino-6-ethylamino- s-triazine), degradation products of atrazine, were observed in the outdoor studies.

Acetamides↗
PubMed1999

Degradation of the nuclear matrix is a common element during radiation-induced apoptosis and necrosis.

Human promyelocytic leukemia (HL60) cells were irradiated with 10 or 50 Gy of X rays and studied for up to 72 h postirradiation to determine the mode of death and assess changes in the nuclear matrix. After 50 Gy irradiation, cells were found to die early, primarily by apoptosis, while cells irradiated with 10 Gy died predominantly by necrosis. Disassembly of the nuclear lamina and degradation of the nuclear matrix protein lamin B occurred in cells undergoing radiation-induced apoptosis or necrosis. However, using Western blotting and a recently developed flow cytometry assay to detect changes in nuclear matrix protein content, we found that the kinetics and mechanisms of disassembly of the nuclear lamina are different for each mode of cell death. During radiation-induced apoptosis, cleavage and degradation of lamin B to a approximately 28-kDa fragment was detected in most cells within 4-12 h after irradiation. Measurements of dual-labeled apoptotic cells revealed that nonrandom DNA fragmentation was evident prior to or concomitant with breakdown of the nuclear lamina. Disassembly of the nuclear lamina during radiation-induced necrosis occurred much later (between 30-60 h after irradiation), and a different cleavage pattern of lamin B was observed. Degradation of the nuclear lamina was also inhibited in apoptosis-resistant BCL2-overexpressing HL60 cells exposed to 50 Gy until approximately 48 h after irradiation. These data indicate that breakdown of the nuclear matrix may be a common element in radiation-induced apoptosis and necrosis, but that the mechanisms and temporal patterns of breakdown of the nuclear lamina during apoptosis are distinct from those of necrosis.

Apoptosis↗