Ten men with Klinefelter's syndrome were studied to assess the effect of testosterone replacement on plasma lipids and apolipoproteins. Measurements taken before the insertion of a testosterone ester implant were compared with those obtained 1 week and 4 weeks later. Mean plasma testosterone, androstenedione, total cholesterol and calculated LDL-cholesterol increased significantly after 1 and 4 weeks. No significant changes were seen in total plasma concentrations of HDL-cholesterol, HDL-cholesterol subfractions 2 and 3 or in apoplipoproteins A-I, A-II or B. A significant correlation was seen between total cholesterol and plasma oestradiol concentrations (Rs = 0.61; P less than 0.001). A significant negative correlation was seen between the concentrations of total testosterone and total triglyceride (Rs = -0.56; P less than 0.005) but not with the other lipid parameters. Testosterone replacement is associated with slight but potentially adverse changes in plasma cholesterol levels.

Epidemiologic evidence indicates an increase in cleft lip with or without cleft palate [CL(P)] in infants of mothers who smoke cigarettes. It appears that the principle mechanism is through carbon monoxide (CO) decreasing the oxygen (O2) available to the embryo. Previous studies have shown that maternal respiratory hypoxia can increase the incidence of CL(P) in mice. The present investigation was designed to analyze the effects of altered levels of CO and O2 in respiratory gases on the incidence of CL(P) in genetically susceptible A/J mice. Results from blood gas analysis, after a 24-hour exposure of pregnant mice during the time of primary palate development, showed that CO levels of 180 ppm in air decrease oxyhemoglobin (%O2Hb) and increased carboxyhemoglobin (%COHb) to slightly above the high end of the range found in human studies of cigarette smokers. Interestingly, the control COHb levels were higher in our CL(P) sensitive mouse strain compared with those of the range of increases found in human smokers, versus nonsmoker studies, and that the increase for treated mice (3x) was at the low end of the range for smokers. Decreasing O2 levels to 10% from 21% (normal percentage in air) more severely decreased %O2Hb and moderately decreased %COHb. At 24 hours of exposure, the incidence of CL(P) and resorption was approximately the same for both the CO and the control groups, but there were significant increases in the incidence of resorptions in the hypoxia group and of CL(P) in relation to the CO group.(ABSTRACT TRUNCATED AT 250 WORDS)

Epidemiologic evidence indicates an increase in cleft lip with or without cleft palate [CL(P)] in infants of mothers who smoke cigarettes. It appears that the principle mechanism is through carbon monoxide (CO) decreasing the oxygen (O2) available to the embryo. Previous studies have shown that maternal respiratory hypoxia can increase the incidence of CL(P) in mice. The present investigation was designed to analyze the effects of altered levels of CO and O2 in respiratory gases on the incidence of CL(P) in genetically susceptible A/J mice. Results from blood gas analysis, after a 24-hour exposure of pregnant mice during the time of primary palate development, showed that CO levels of 180 ppm in air decreased oxyhemoglobin (%O2Hb) and increased carboxyhemoglobin (%COHb) to slightly above the high end of the range found in human studies of cigarette smokers. Interestingly, the control COHb levels were higher in our CL(P) sensitive mouse strain compared with those of the range of increases found in human smokers, versus nonsmoker studies, and that the increase for treated mice (3x) was at the low end of the range for smokers. Decreasing O2 levels to 10% from 21% (normal percentage in air) more severely decreased %O2Hb and moderately decreased %COHb. At 24 hours of exposure, the incidence of CL(P) and resorption was approximately the same for both the CO and the control groups, but there were significant increases in the incidence of resorptions in the hypoxia group and of CL(P) in relation to the CO group. A statistically significant increase in CL(P), but not resorptions was found for a longer CO treatment time (48 hours vs. 24 hours of exposure). Also, an increase in the severity of clefting was noted with the carbon monoxide treated groups having more bilateral CL(P) than unilateral CL(P). The low incidences of CL(P) in the control groups prevented statistical analysis, although results from other studies indicate that the increased severity is real. CO exposure longer than 48 hours seems to give no additional increase in clefting incidence. We conclude that chronic exposure to moderate levels of CO increases the incidence and severity of CL(P) in A/J mice. The possible additional effects of nicotine in cigarette smoke and of other confounding factors related to smoking and CL(P) are discussed.