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W C Eastin

Publications and source records attributed to W C Eastin.

10 recordsLinked to original sources
PubMed1991

Evidence for a common genetic pathway controlling susceptibility to mouse skin tumor promotion by diverse classes of promoting agents.

The present study has compared different mouse stocks and strains with known sensitivity to phorbol ester skin tumor promotion for their sensitivities to skin tumor promotion by a prototypic organic peroxide (benzoyl peroxide, BzPo) and anthrone (chrysarobin, Chr) tumor promoter. Following initiation with either 7,12-dimethylbenz(a)anthracene and/or N-methyl-N'-nitro-N-nitrosoguanidine, groups of mice were promoted with several different doses of each promoting agent. Among mice selectively bred for sensitivity to phorbol ester promotion, the order of sensitivity to BzPo was inbred SENCAR (SSIn) greater than SENCAR greater than CD-1. With Chr as the promoter, the order of sensitivity was SENCAR greater than SSIn greater than CD-1. Concurrent tumor promotion experiments examined the responsiveness of two common inbred mouse strains, DBA/2 and C57BL/6. The phorbol ester-responsive mouse strain, DBA/2, was more sensitive to skin tumor promotion by Chr than was C57BL/6 at all doses tested but was clearly less sensitive than both SENCAR and SSIn mice. Finally, DBA/2 and C57BL/6 mice were similar in their responsiveness to BzPo promotion, but again both of these inbred strains were significantly less sensitive than were SSIn and SENCAR mice to this organic peroxide type of skin tumor promoter. Histological evaluations comparing SENCAR and C57BL/6 mice revealed that a major difference between these strains in response to multiple Chr and BzPo treatments was in the inflammatory response (measured by edema formation). Unlike 12-O-tetradecanoylphorbol-13-acetate, Chr and BzPo did not induce dramatic differences in the epidermal hyperplasia (as measured by epidermal thickness) in these two mouse lines. The results presented in this paper suggest that there is a common pathway controlling susceptibility to skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate, BzPo, and chrysarobin. These results are discussed in terms of a possible genetic model(s) for skin tumor promotion in mice.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1987

Intestinal absorption of two glucose analogues in rats of different ages.

Intestinal absorption of nutrients and xenobiotics has been suggested to change during aging. Transport processes were examined using nonmetabolizable glucose analogues as markers in an in situ single pass intestinal perfusion procedure. Male Fischer 344 rats of 2, 4, 10, 16, and 27 months of age were used in this study. At least 7 rats were used per age group. Net active and passive transport were estimated using 0.85% NaCl solutions containing [14C]-3-O-methylglucose (3OMG) and [3H]-2-deoxy-D-glucose (2DG) and phenol red as nonabsorbed volume marker. Rats were anesthetized and approximately 30 cm of jejunum was perfused for 30 min. Final glucose analogue concentrations were corrected for volume changes, and compared with initial concentrations. Changes in marker concentrations were normalized to the dry weight of the perfused intestinal segment. Concurrent exposure to both glucose analogues allowed simultaneous monitoring of active and passive components. Under these conditions, there was no significant change in the net transport of 2DG, a compound absorbed by nonspecific processes (range 17-33 mumoles/g/h). In the same animals, the rate of net 3OMG absorption, an actively transported compound, was generally an order of magnitude greater than 2DG. In addition, net 3OMG absorption was significantly (p less than .05) decreased in the 16- and 27-month-old rats (237 and 181 mumoles/g/h) compared with the 2-, 4- and 10-month-old animals (325, 364 and 398 mumoles/g/h, respectively). There appears to be a gradual decrease in net active transport of glucose with age. The mechanism responsible for this age-related change remains to be explained.

3-O-Methylglucose↗
PubMed1982

Effects of lindane, paraquat, toxaphene, and 2,4,5-trichlorophenoxyacetic acid on mallard embryo development.

The effects were determined of externally treating mallard (Anas platyrhynchos) eggs with two insecticides (lindane and toxaphene) and two herbicides (paraquat and 2,4,5-T) with formulations and concentrations similar to field applications. Paraquat was the most embryotoxic of the four compounds regardless of the type of vehicle. The LC50 for paraquat was 1.5 lb of active ingredient/acre in aqueous emulsion and 0.1 lb/acre in the oil vehicle. The other compounds had LC50's that were several orders of magnitude higher. Both paraquat and toxaphene caused some mortality at 1/2 of the field level of application. Paraquat impaired growth and was slightly teratogenic at 1/2 of the field level of application, but required higher concentrations (1.5 to 3 times the field level) to produce brain and visceral defects. Lindane was teratogenic, resulting in multiple defects but only at doses that were greater than five times the field level of application. Toxaphene resulted in defects of the joints at doses close to or exceeding the LC50. The herbicide 2,4,5-T resulted in few toxic effects and relatively few abnormal survivors with gross defects. The overall embryotoxicity with either vehicle was paraquat greater than lindane greater than toxaphene greater than 2,4,5-T on a lb per acre basis. However the potential hazard at exposures of up to five times the field level of application was paraquat greater than toxaphene; neither lindane nor 2,4,5-T constituted much of a hazard. Both paraquat and lindane were more toxic on lb-per-acre basis when administered in oil vehicle but only paraquat represented a potential hazard at five times the field level of application.

2,4,5-Trichlorophenoxyacetic Acid↗
PubMed1982

Organophosphate inhibition of avian salt gland Na, K-ATPase activity.

1. Adult black ducks (Anas rubripes) were given freshwater or saltwater (1.5% NaCl) for 11 days and half of each group was also given an organophosphate (17 p.p.m. fenthion) in the diet on days 6-11. 2. After 11 days, ducks drinking saltwater had lost more weight and had higher plasma Na and uric acid concentrations and osmolalities than birds drinking freshwater. 3. Saltwater treatment stimulated the salt gland to increased weight and Na, K-ATPase activity. 4. Fenthion generally reduced plasma and brain cholinesterase activity and depressed cholinesterase and Na, K-ATPase activities in salt glands of birds drinking saltwater.

Animals↗
PubMedDate not supplied

Disposition of 4,4'-thiobis(6-t-butyl-m-cresol) in rats.

The absorption, distribution, metabolism, and excretion of 14C-labeled 4,4'-thiobis(6-t-butyl-m-cresol) (TBBC) was studied in male rats. Oral treatment showed a dose-related decrease in the rate of absorption due to a dose-related increase in retention time in the stomach. TBBC was incompletely absorbed after oral treatment, although the rate of absorption was proportional to the dose once the compound reached the small intestine. TBBC was rapidly distributed throughout the body with the liver being the major tissue depot. Significant amounts of the compound were also present in blood, muscle, skin, and adipose tissue. TBBC was initially rapidly cleared from all tissues except adipose, although a small percentage of the total dose tended to persist in liver and skin. Over half of the compound was excreted the first day, primarily via the bile into the feces. Little TBBC-derived radioactivity appeared in the urine. Metabolites of TBBC were present in the tissues at early times after administration, but were rapidly excreted. The major metabolite(s) appeared to be glucuronide conjugates of the parent compound. Thus, TBBC, an important antioxidant in the rubber and plastic industries, would tend to accumulate in liver and lipid-rich tissues upon chronic exposure, which if by the oral route, could also result in direct damage to the gastrointestinal tract.

Animals↗