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J B Vaught

Publications and source records attributed to J B Vaught.

31 records · Page 2Linked to original sources
PubMed1979

Phenacetin studies.

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Acute Kidney Injury↗
PubMed1979

Effect of smoking on benzo(a)pyrene metabolism by human placental microsomes.

Placentas were collected at term from a series of 21 women. Thirteen were smokers, and eight were nonsmokers. Microsomes were prepared and used in the following studies of benzo(a)pyrene metabolism: aryl hydrocarbon, hydroxylase, epoxide hydrase, high-pressure liquid chromatographic analysis of benzo(a)pyrene metabolites, and DNA binding. DNA-binding adducts were further characterized by Sephadex LH-20 chromatography. Aryl hydrocarbon hydroxylase activity was much higher in smokers than in nonsmokers. Epoxide hydrase activity with styrene oxide as the substrate showed no difference between smokers and nonsmokers. High-pressure liquid chromatographic analysis showed much greater formation of dihydrodiols, quinones, and phenols by microsomes from smokers. The amount of benzo(a)pyrene-7,8-dihydrodiol was almost equal to the amount of phenols produced by the microsomes of the smokers. Sephadex LH-20 analysis of DNA binding resulted in only one major benzo(a)pyrene-DNA adduct when microsomes from smokers were used; this peak corresponds to benzo(a)pyrene 7,8-diol-9, 10-oxide bound to DNA nucleoside(s).

Aryl Hydrocarbon Hydroxylases↗
PubMed1978

Comparison of benzo[a]pyrene metabolism by human peripheral blood lymphocytes and monocytes.

Here we report a more sensitive high-pressure liquid chromatographic (HPLC) assay of benzo[a]pyrene (BP) metabolites elaborated by human monocytes and lymphocytes using only 10 X 10(6) cells for HPLC analysis. The major metabolites formed by both lymphocytes and monocytes were 3-hydroxy-BP, 9-hydroxy-BP and quinones. BP-dihydrodiols were also found by HPLC analysis, the major one being BP-7,8-dihydrodiol for both cell types. In addition, a peak slightly more polar than 9,10-dihydrodiol was formed by lymphocytes. The 7,8-diol peak was eliminated by the addition of 1,1,1-trichloropropene oxide to the incubation mixture. The presence of alpha-napthoflavone resulted in an overall decrease in metabolite production.

Benzopyrenes↗
PubMed1976

Breakage of human cell DNA after exposure to 3-methylcholanthrene-11,12-oxide.

Damage to and repair of DNA isolated from human neonatal and fetal skin cells were measured by alkaline sucrose gradient analysis. 3-Methylcholanthrene did not induce single-strand breaks in DNA of the cells in culture, whereas the 11,12-oxide of 3-methylcholanthrene was very effective in this regard. The cis-1,2-dihydroxy, trans-11,12-dihydroxy, and cis-11,12-dihydroxy derivatives of 3-methylcholanthrene exerted little effect. The breaks in DNA caused by 3-methylcholanthrene oxide occurred during a 60-min incubation period and were repaired during the following 60 min. Methylmethane sulfonate also induced breaks in the DNA within 60 min.

Cells, Cultured↗
PubMedDate not supplied

The role of agricultural pesticide use in the development of non-Hodgkin's lymphoma in women.

Non-Hodgkin's lymphoma has been found to be associated with agricultural pesticide use in men, but little is known about the risk in women. In a recent population-based, case-control study conducted in eastern Nebraska, no increased risk of non-Hodgkin's lymphoma was found in women who had ever lived or worked on a farm (odds ratio [OR] = 1.0). Neither the use of insecticides (OR = 0.8) nor herbicides (OR = 0.7) on the farm was associated with non-Hodgkin's lymphoma; however, the number of women who mixed or applied pesticides was small, particularly in comparison to men on farms. Small nonsignificant associations were observed among the women who personally handled insecticides (OR = 1.3) or herbicides (OR = 1.2). Women who personally handled organophosphate insecticides had a significant 4.5-fold increased risk of non-Hodgkin's lymphoma. Use of chlorinated hydrocarbon insecticides was associated with an OR of 1.6; however, the use on dairy cattle was associated with a 3-fold increased risk. Pesticide-related risks were greater among women with a family history of cancer, particularly a history of lymphatic or hematopoietic cancer among first-degree relatives.

Adult↗