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Biomedical subjects

M W Anderson

Publications and source records attributed to M W Anderson.

At least 145 records · Page 8Linked to original sources
PubMed1983

Effect of aspirin and indomethacin on the formation of benzo(a)pyrene-induced pulmonary adenomas and DNA adducts in A/HeJ mice.

Previous results in various in vitro systems suggest that prostaglandin endoperoxide synthetase (PES) could serve as either an alternative or an additional enzyme to the cytochrome P-450-dependent monooxygenases for the formation of mutagenic, cell-transforming, and DNA-binding metabolites of carcinogens. To test this hypothesis in vivo, we examined the effect of PES inhibitors on benzo(a)pyrene (BP)-induced pulmonary adenoma and BP metabolite:DNA adduct formation in A/HeJ mice. Animals were treated with a dosage regimen of aspirin which inhibited PES but had no effect on the cytochrome P-450-dependent oxidation of 7,8-dihydrodihydroxybenzo(a)pyrene. Aspirin did not significantly alter the number of pulmonary adenomas per mouse at either dose of BP (6.0 and 3.0 mg per mouse, administered twice, 2 weeks apart). In addition, aspirin treatment did not depress the in vivo formation of BP metabolite:DNA adducts in lung or liver at either dose of BP (6.0 and 0.06 mg/mouse). The lower dose of BP was used in the adduct study to assess the effect of aspirin at a more environmental exposure level of BP. Treatment with indomethacin, another PES inhibitor, also did not reduce the pulmonary BP metabolite:DNA adduct levels. The failure of PES inhibitors to reduce the number of pulmonary adenomas and BP metabolite:DNA adduct levels suggests that cooxidation of BP during prostaglandin biosynthesis may not play a significant role in BP-induced pulmonary adenomas.

Adenoma↗
PubMed1982

Triiodothyronine thyrotoxicosis complicating primary hypothyroidism in a patient with autoimmune thyroiditis.

It is increasingly recognized that autoimmune thyroiditis can have a multifaceted presentation. Documented triiodothyronine thyrotoxicosis developed in a patient with a six-year history of primary hypothyroidism that was left untreated. Serologic and cytologic evidence confirmed the thyroid dysfunction as being on an autoimmune basis. Chronic lymphocytic thyroiditis may be seen with hyperthyroidism, hypothyroidism, or euthyroidism, and in an individual patients, spontaneous progression from one metabolic state to another may occur.

Autoimmune Diseases↗
PubMed1982

A study of the fate of gum karaya in the rat.

Rats were fed a diet containing 5% gum karaya for 24 h and faeces and urine were collected over 72 h. Faeces were examined, after methanolysis, by gas chromatography--mass spectometry and the quantity and monosaccharide composition of the faecal polysaccharide were compared with the dose and original composition of the gum polysaccharide. Gum-derived rhamnose was not found in the urine. Indications of minor quantitative changes in composition but no evidence of extensive degradation or absorption of gum polysaccharide, were found.

Animals↗
PubMed1982

Hospital pharmacy computer systems--1982.

Results of a survey of hospital pharmacy computer systems vendors are reported. A questionnaire was mailed to 317 possible vendors of hospital pharmacy computer systems in August 1982. Of the 89 companies responding, 30 stated that they marketed a hospital pharmacy system. The results are tabulated in this paper according to general system information, system hardware, system software, and system features. The most common classification of the responding companies was the health-system corporation; second most common was pharmacy computer system companies. Twenty companies have marketed their systems for two years or longer. Sixteen companies now claim to have contracts with more than 20 health-care institutions. The survey results are offered as a guide for comparing the similarities and differences among various vendors of hospital pharmacy computer systems.

Computers↗
PubMed1982

Effect of butylated hydroxyanisole, alpha-angelica lactone, and beta-naphthoflavone on benzo(alpha)pyrene:DNA adduct formation in vivo in the forestomach, lung, and liver of mice.

The effects of alpha-angelica lactone (alpha-AL), butylated hydroxyanisole (BHA), and beta-naphthoflavone (beta-NF) on the amount of benzo(alpha)pyrene (BP) metabolite:DNA adducts formed in the forestomach, lung, and liver of ICR/Ha mice were investigated 48 hr after p.o. administration of BP. BP was administered to mice in amounts known to result in BP-induced neoplasia in certain tissues. Analysis of deoxyribonucleosides by high-pressure liquid chromatography showed that several BP metabolite:DNA adducts were formed in each tissue examined. The major identified adduct in each tissue cochromatographed with the (+/-)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(alpha)pyrene (BPDEI):deoxyguanosine adduct. The (+/-)-7 beta,8 alpha-dihydroxy-9 beta,10 beta-epoxy-7,8,9,10-tetrahydrobenzo(alpha)pyrene (BPDEII):deoxyguanosine adduct was detected in each of the tissues. As a percentage of total DNA-associated radioactivity, the BPDEI:DNA and BPDEII:DNA adducts accounted for 14% in the forestomach, 39% in the lung, and 3% in the liver. Another adduct, possibly derived from BP:phenol(s), was detected in lung and liver. Early eluting unidentified DNA-associated radioactivity was also present in each of the tissues and accounted for the majority of the radioactivity (88%) in forestomach, 57% in lung, 97% in liver). Although total DNA-associated radioactivity in liver was approximately 15-fold higher than in lung and 5-fold higher than in forestomach, the specific activities of the BPDEI:adducts and of the BPDEII:adducts were approximately the same in these organs. Addition of alpha-AL or BHA to the diet inhibited BPDEI:DNA adduct formation in the forestomach and liver but not in the lung. The effect of beta-NF was not tissue specific; this aryl hydrocarbon hydroxylase inducer decreased markedly (80 to 90%) BPDEI:DNA adduct formation in all three tissues. The radioactivity associated with the early eluting peaks was also reduced when associated with the early eluting peaks was also reduced when alpha-AL, BHA, or beta-NF was fed to the mice. The inhibition of BPDEI:DNA and BPDEII:DNA adduct formation by alpha-AL, BHA, and beta-NF is discussed in relation to similar studies where these compounds inhibited BP-induced neoplasia.

4-Butyrolactone↗
PubMed1981

Dermatoglyphic feature of myocardial infarction patients.

An association reported between certain dermatoglyphic features and myocardial infarction (MI) in Japanese males is investigated using a sample of Caucasian males. The frequencies in each of the four Galtonian pattern types (arch, ulnar loop, radial loop, whorl) defined on each of the ten primary digital pattern areas, as well as several synthetic fields for the MI and control groups, are compared. Total and absolute finger ridge count for the same pattern areas in the two samples are similarly studied. No differences in the distributions of these features significant at the 0.01 level or less could be demonstrated between the MI and control samples. A search for combinations of features to correctly classify the individuals into the two groups was similarly inconclusive. Differences in sample size and racial homogeneity that may account for this failure to reproduce the results of the study of Japanese males are discussed. Finally, statistics describing the distributions of the dermatoglyphic features in the test and control samples are presented for comparison with future investigations.

Dermatoglyphics↗
PubMed1981

Parotid gland pathophysiology after mixed gamma and neutron irradiation of cancer patients.

Electrolyte and protein concentrations were measured in parotid saliva samples obtained from patients receiving localized, fractionated, neutron and gamma irradiation for the treatment of cancer. Salivary sodium chloride concentration increased transiently but then usually decreased to preirradiation values after 2 weeks of therapy. There were concurrent decreases in salivary flow rate, pH, and bicarbonate concentration. The decreases in sodium chloride concentration and flow rate are inconsistent with a previously suggested, irradiation-induced ductal sodium resorption defect. The findings contribute toward understanding how salivary gland physiology is altered in irradiation injury.

Aged↗
PubMed1981

Inhibition in vivo of the formation of adducts between metabolites of benzo(a)pyrene and DNA by aryl hydrocarbon hydroxylase inducers.

The lungs of A/HeJ mice are susceptible to benzo(a)pyrene (BP)-induced neoplasia whereas the livers are resistant. Following p.o. administration of a carcinogenic dose of [3H]BP, radioactivity was associated with the DNA of both lung and liver. Analysis of the deoxyribonucleosides by high-pressure liquid chromatography showed that the major adduct in both tissues chromatographed as the (+/-)-7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDEI)-deoxyguanosine adduct. The (+/-)-7 beta, 8 alpha-dihydroxy-9 beta, 10 beta-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDEII)-deoxyguanosine adduct was 9 to 15% of the BPDEI adduct in both lung and liver. Although total DNA-associated radioactivity was approximately 12-fold higher in liver than in lung, the specific activities of the BP diol-epoxide adducts were approximately the same in these organs. Treatment of animals with beta-naphthoflavone (beta NF), an inhibitor of pulmonary adenoma formation, markedly decreased the amount of the BDPEI and BPDEII adducts in the lung and the liver. The decrease in the amount of these adducts in the lung correlates with the inhibition of tumorigenesis by beta NF. The inhibition of total DNA-associated radioactivity was significantly less than the BP diol-epoxide adducts. Thus, beta NF appears to inhibit BP-induced pulmonary neoplasia by reducing the amount of the BPDEI-deoxyguanosine adduct. Other inducers of aryl hydrocarbon hydroxylase were also tested for their effect on the formation of BP-deoxyribonucleoside adducts. Both 2,3,7,8-tetrachlorodibenzo-p-dioxin and Aroclor 1254 significantly reduced the amount of the BPDEI adduct in both lung and liver. These data would suggest that both 2,3,7,8-tetrachlorodibenzo-p-dioxin and Aroclor 1254, like beta NF, should protect against BP-induced pulmonary neoplasia. The effects of aryl hydrocarbon hydroxylase inducers on the binding of BP to DNA in vivo markedly contrast with their effect in vitro. Treatment of animals with aryl hydrocarbon hydroxylase inducers stimulates the formation of BP diol-epoxide adducts in vitro. The reason for the differences between our in vivo results and those predicted from in vitro studies is unclear.

Animals↗
PubMed1981

Inhibition in vivo of the formation of adducts between metabolites of benzo(a)pyrene and DNA by butylated hydroxyanisole.

Antioxidants have been shown to inhibit the carcinogenic effects of a variety of chemical carcinogens. For example, the phenolic antioxidant butylated hydroxyanisole (BHA) has been shown to be a potent inhibitor of benzo(a)pyrene (BP)-induced neoplasia in mouse lung and forestomach. The objective of the present study was to determine whether or nt BHA, under conditions known to result in inhibition of BP-induced neoplasia, affects the formation of BP metabolite:DNA adducts. Following p.o. administration of a carcinogenic dose of [3H]BP to A/HeJ mice, radioactivity was detected in the DNA of both lung and liver. Analysis of the deoxyribonucleosides by high-pressure liquid chromatography showed that the major adduct in both tissues cochromatographed with the (+/-)-7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDEI):deoxyguanosine adduct. The 7 beta, 8 alpha-dihydroxy-9 beta, 10 beta-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BPDEII):deoxyguanosine adduct was 10 to 15% of the BPDEI adduct in both lung and liver. Another adduct, possibly derived from BP phenol(s), was also detected in lung and was 10 to 20% of the BPDEI adduct. Treatment of animals with BHA decreased the amount of the BPDEI adduct in the lung and the liver approximately 55 and 75%, respectively. The decrease in the amount of this adduct in the lung appears to correlate with the inhibition of pulmonary adenoma formation (L. W. Wattenberg, J. Natl. Cancer Inst., 50: 1541-1544, 1973; J. L. Speier, L. K. Lam, and L. W. Wattenberg, J. Natl. Cancer Inst., 60: 605-609, 1978). Thus, BHA appears to inhibit BP-induced pulmonary adenoma formation by inhibiting the amount of the BPDE:DNA adducts formed in lung. Possible mechanisms by which BHA treatment inhibits the formation of BPDE:DNA adducts are discussed.

Animals↗
PubMed1979

Inhibition of pulmonary prostaglandin metabolism by exposure of animals to oxygen or nitrogen dioxide.

The effects of exposure of animals to 100% O2 and NO2 on the rate of prostaglandin metabolism by lung and kidney were studied in vitro. Exposure of guinea pigs to 100% O2 for 48 h inhibited the metabolism of prostaglandin F2 alpha by both NAD+- and NADP+-dependent prostaglandin dehydrogenase in lung, but had no effect on the metabolism in kidney. Succinate dehydrogenase, but not glucose 6-phosphate dehydrogenase, in guinea-pig lung was inhibited by exposure to 100% O2. Exposure to 46 p.p.m. but not 16 or 29 p.p.m. NO2 for 6 h inhibited guinea-pig lung prostaglandin dehydrogenase in vitro. The inhibition of pulmonary prostaglandin dehydrogenase by exposure to 100% O2 or to 49 p.p.m. NO2 was dependent on the duration of exposure, but returned to control values within 7 days after cessation of the exposure. The pulmonary transport system responsible for removing circulating prostaglandins from the blood was not affected by exposure to 100% O2 as measured by using the isolated perfused lung. Kinetic analysis of the inhibition of pulmonary prostaglandin dehydrogenase activity in guinea pig exposed to 100% O2 showed non-competitive inhibition with respect to both prostaglandin F2 alpha and NAD+, which suggests destruction or inactivation of the enzyme. Pulmonary prostaglandin dehydrogenase appears to be inhibited by exposure to oxidant gases, which may lead to elevated prostaglandin concentrations in the lungs or in the systemic circulation.

15-Oxoprostaglandin 13-Reductase↗