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E A Reed

Publications and source records attributed to E A Reed.

12 recordsLinked to original sources
PubMed1992

DNA adduct formation in mice following dermal application of smoke condensates from cigarettes that burn or heat tobacco.

A prototype cigarette that heats tobacco (test cigarette), developed by R.J. Reynolds Tobacco Company, has yielded consistently negative results in several in vivo and in vitro genetic toxicology tests. The objective of the present study was to evaluate the potential of cigarette smoke condensate (CSC) from the test cigarette to induce DNA adducts in mouse tissues and compare the results with those obtained with CSC from a reference tobacco-burning cigarette (1R4F). CD-1 mice were skin-painted with CSC from reference and test cigarettes three times a week for 4 weeks. The highest mass of CSC applied was 180 mg "tar" per week per animal for both reference and test cigarette. DNA adducts were analyzed in skin and lung tissues using the 32P-postlabeling method with the P1 nuclease modification. Distinct diagonal radioactive zones (DRZ) were observed in the DNA from both skin and lung tissues of animals dosed with reference CSC, whereas no corresponding DRZ were observed from the DNA of animals dosed with either test CSC or acetone (solvent control). The relative adduct labeling (RAL) values of skin and lung DNA from reference CSC-treated animals were significantly greater than those of the test CSC-treated animals. The RAL values of the test CSC-treated animals were no greater than those of solvent controls. The negative results in DNA adduct assays with test CSC are consistent with all previous results of in vivo and in vitro genetic toxicology testing on this cigarette and provide additional evidence that smoke condensate from the test cigarette is not genotoxic.

Animals↗
PubMed1975

Influence of increased circulating levels of splanchnic lysosomal enzymes on the response to myocardial ischemia.

The ability of increased circulating activities of lysosomal hydrolases to disrupt myocardial cellular membranes was studied in anesthetized cats. Increased activities of lysosomal hydrolases were achieved by splanchnic artery occlusion (SAO) shock or by infusion of liver extract (LE). Myocardial ischemia (MI) was produced by ligation of the left coronary artery. Coronary artery ligation resulted in sustained S-T segment elevation associated with significant increases in plasma creatine phosphokinase (CPK) activity within 5 hours. Combinations of SAO or LE infusion did not modify the increase in either the plasma CPK activity or the S-T segment following MI. However, SAO shock or infusion of LE increased CPK loss from normal and ischemic myocardium, the loss being greater when MI was combined with infusion of LE or SAO shock. Similarly, MI plus SAO shock increased the loss of the lysosomal protease cathepsin D from normal and ischemic myocardial tissue. Moreover, cats subjected to MI and given LE inhibited increased mortality and decreased clearance of infused lysosomal hydrolases. These results indicate that conditions affecting increased plasma levels of hydrolases promote increased disruption of normal and ischemic myocardial tissue. These findings are consistent with the concept that hydrolases originating in the splanchnic viscera during shock play a role in enhancing damage to normal and ischemic myocardial tissue following coronary artery occlusion.

Abdomen↗