Serum and Plasma Markers of Nutritional Status in Children Infected with the Human Immunodeficiency Virus

Objective To determine whether reduced serum or plasma protein and micronutrient levels are common in children infected with the human immunodeficiency virus (HIV) and whether these levels are different in children with growth retardation compared to those with normal growth.

Subjects Children were separated into three groups: (a) HIV-infected with growth retardation (HIV+Gr); (b) HIV-infected with normal growth (HIV+); (c) HIV-uninfected with normal growth (HIV-). All children were afebrile and free of acute infection at the time of study. During a 24-hour stay in the Pediatric Clinical Research Unit, blood was drawn for analysis of total protein, albumin, zinc, selenium, and vitamin A levels; growth measurements were obtained; and dietary intake was assessed by 24-hour weighed food intake and 24-hour dietary recall.

Statistical analysis Mean differences between groups were assessed by analysis of variance, and differences in the frequency of nutrient deficiency were determined by χ² analysis.

Results Thirty-eight children between 2 and 11 years of age were studied: 10 HIV+Gr, 18 HIV+, and 10 HIV-. No statistically significantly differences were noted in mean levels of albumin, prealbumin, zinc, and selenium. Mean serum level of vitamin A was significantly higher in the HIV+Gr group than in the other two groups. There were no significant differences between groups in the frequency of deficiency for any nutrient studied. Mean energy and nutrient intake was similar among groups.

Applications/conclusions Abnormal serum or plasma protein or micronutrient levels were uncommon in this cohort of HIV-infected children, even in children with growth retardation. Routine monitoring of the level of proteins and micronutrients studied is unnecessary in the absence of specific clinical indicators of deficiency. J Am Diet Assoc. 1997-97:1377-1381.     

Effects of the Long-Term Depletion of Reduced Glutathione in Mice Administered L-Buthionine-S,R-sulfoximine

Effects of the Long-Term Depletion of Reduced Glutathione inMice Administered L-Buthionine-S,R-sulfoximine. SUN, J. D.,RAGSDALE, S. S., BENSON, J. M., AND HENDERSON, R. F. (1985).Fundam. Appl. Toxicol.. 5,913-919. Previous methods to depletein vivo concentrations of reduced glutathione (GSH) have notbeen able to lower tissue GSH levels for extended periods, havebeen toxic, and can alter the metabolism of xenobiotics. A possiblealternative to lower in vivo concentrations of GSH may be theuse of buthionine-S,R-sulfoximine (BSO) in the drinking waterof laboratory animals to inhibit the biosynthesis of GSH. Ithas been previously reported that 20 mM BSO in the drinkingwater given to mice was able to lower GSH levels in a varietyof tissues after 15 days. In order to more fully characterizethe in vivo depletion of GSH in tissues by ingestion of BSOand determine if this method would be suitable in studies requiringdepressed levels of GSH for extended periods, we added differentamounts of this agent to the drinking water given to mice forvarious times up to 28 days. We found that ingested BSO at thehighest concentrtion used in drinking water (30 mM) was ableto maximally lower GSH concentrations in mouse lungs, lung lavagefluid, liver, kidneys, and blood to 59.0 ? 3.6%, 35.0 ? 5.1%,44.3 ? 1.5%, 69.5 ? 3.9%, and 70.0 ? 6.0% of control mice, respectively,for up to 28 days. These lowered concentrations of tissue GSHreturned to control levels after mice were returned to untreateddrinking water for 7 days. The potential toxicity of such treatmentswas also evaluated. Levels of alkaline phosphatase, lactatedehydrogenase, glucose-6-phosphate dehydrogenase, glutathioneperoxidase, and glutathione reductase in lungs and lung lavagefluid, and total and differential cell counts from lung lavagefluid were not different between control and BSO-treated mice.This showed that BSO treatment did not produce indications oflung injury as measured by these biochemical parameters. Serumaspartyl transferase and -glutamyl transpeptidase activitieswere unaffected by the BSO treatments, indicating normal liverfunctions. Lung and liver cytochrome P-450 concentrations werealso not different between controls and BSO-treated animals.Thus, BSO in the drinking water of mice was able to effectivelylower in vivo levels of GSH without eliciting aCUte toxic responses.     

Diesel Exhaust Is Not a Pulmonary Carcinogen in CD-1 Mice Exposed under Conditions Carcinogenic to F344 Rats

Differences among laboratory animal species in the pulmonarycarcinogenicity of chronic inhalation exposure to diesel exhausthave raised several important interpretive issues. Under similarheavy exposure conditions, it is clear that diesel exhaust isa pulmonary carcinogen in rats, but not in Syrian hamsters.Previous reports give conflicting views of the response of mice,which is presently considered equivocal. This report describescarcinogenicity results from a bioassay of CD-1 mice conductedin parallel with a previously reported bioassay of F344 rats(Mauderly et al. (1987) Fundam. Appl. Toxicol. 9, 208–221).Exposure to whole diesel exhaust 7 hr/day, 5 days/week for 24months at soot concen trations of 0.35, 3.5, or 7.1 mg/m³ causedaccumulations of soot in mouse lungs similar to those in lungsof rats and, like the results from rats, did not significantlyaffect survival or body weight. In contrast to the dose-relatedneoplastic response of rats, however, the exposures of micedid not increase the incidence of lung neoplasms. This findingis consistent with other data showing that mice, as well asSyrian hamsters, differ from rats in their lung neoplastic andnonneoplastic responses to heavy, chronic inhalation exposureto diesel exhaust soot and several other particles. Althoughrodents serve as useful indicators of potential human carcinogenichazards, it is not yet clear which, if any, rodent species havelung neoplastic responses that are useful for quantitative predictionsof human lung cancer risk from chronic inhalation of poorlysoluble, respirable particles.