Release of atrazine ((14)C) from two undisturbed submerged sediments over a two-year period.

Through water erosion and runoff, sediment-adsorbed atrazine can undergo sedimentation and accumulation at the bottom of water bodies and become potential sources of atrazine to the water column. The purpose of this study is to determine the fate and release of atrazine ((14)C) to the water column from two simulated undisturbed submerged sediments at two temperature treatments (5 and 24 degrees C) over a 2-year period. Atrazine residue ((14)C) was released from the two sediments and was, primarily, diffusing from the sediment pore water to the water columns. The amount released was affected by sediment type and is related to the sediment's adsorption/desorption capacity. Larger amounts of residue ((14)C) were released to the water columns at 5 degrees C than at 24 degrees C. Atrazine degraded in the shallow submerged anaerobic sediment's water columns over the 2-year period. Less than 2% (percent of applied in atrazine equivalent) of extractable atrazine and metabolites remained in the sediment after 2 years. The amount of nonextractable atrazine residue ((1)(4)C) was significantly higher in sediments at 24 degrees C than at 5 degrees C. In conclusion, atrazine accumulating in shallow undisturbed submerged sediments from nonpoint sources would most likely degrade and/or become nonextractable over time and would have a low probability of becoming a significant source to the water body. The conditions where accumulation and future release of atrazine have a greater potential to occur are under very cold temperatures with low adsorption capacity sediments.

The effect of high dose vitamin A on the morphology and proliferative activity of xenograft lung and head and neck cancer.

In vitro studies have suggested that vitamin A lowers invasive potential of squamous cell carcinoma. Epidemiological data have also indicated that high dose vitamin A may improve survival in patients with previously resected lung carcinoma. To our knowledge, no studies have attempted to test the in vivo effect of vitamin A on the morphology and growth rate of lung and head and neck cancer. Freshly resected tumor cell suspensions were obtained by ex vivo fine needle aspiration and injected subcutaneously in duplicate in athymic male nude mice. Two to six weeks post-engraftment tests and controls were separated for each xenograft. Mice with test xenografts were given water soluble vitamin A (Aquasol ATM, Astra pharmaceutical, Westborough, MA, U.S.A) at a dose of 10,000 U/Kg/day intraperitoneally for 6 to 10 weeks (median 8 weeks). One to two hours prior to sacrifice bromodexouridine (BrdU) was injected intraperitoneally to assess the S-phase fraction in both test and control xenografts. Blood vitamin A levels in test and control animals were measured after sacrifice using high performance liquid chromatography (HPLC). Sections of test and control xenografts were routinely stained to assess morphologic differentiation and mitotic counts. Unstained sections of xenografts were immunostained by the antibody to BrdU to test for BrdU labeling index (BLI) reflecting S-phase fraction (SPF) and also by the MIB-1 antibody to assess proliferative activity. Eighteen tumors were studied. These included 9 squamous cell carcinomas of the lung, 5 squamous cell carcinomas of the head and neck, and 4 adenocarcinomas of the lung. Blood levels of vitamin A in test animals were 7 to 23 times those of the control animals (median 13 times). Neovascularization of the xenografts was seen in all cases. The morphology and mitotic activity of the test and control xenografts showed no significant difference. SPF and proliferative activity measured by BrdU and MIB-1 immunolabelling respectively showed no significant difference between test and control xenografts. Our study suggests that there is no significant in vivo effect of high dose vitamin A on the morphology and growth rate of xenografted non small cell carcinoma of the lung or squamous cell carcinoma of the head and neck.