Human Control Subjects Research Articles

IFN-gamma enhances osteoclast generation in cultures of peripheral blood from osteopetrotic patients and normalizes superoxide production.

Interferon-gamma (IFN-gamma) treatment increases osteoclastic bone resorption in vivo in patients with malignant osteopetrosis (OP). The treatment effect was studied in vitro in osteoclasts generated by culturing peripheral white blood cells (PWBC) from OP patients and normal human control subjects. Osteoclasts were treated with or without IFN-gamma prior to the end of the culture period. Osteoclasts from normal subjects were large in size (161 +/- 18 microm in diameter) with >10 nuclei per osteoclast. These cells showed intense staining for tartrate-resistant acid phosphatase (TRAP), expressed abundant calcitonin receptors (CTR), and formed numerous resorption pits on bovine bone slices, indicative of authentic osteoclasts. In contrast, similarly cultured osteoclasts from OP patients were smaller in size (18 +/- 3 microm in diameter), with 2-3 nuclei per osteoclast, and stained lightly for TRAP. However, IFN-gamma treatment of osteoclasts from OP patients resulted in the formation of larger osteoclasts (171 +/- 33 microm in diameter) with >10 nuclei per cell, similar in appearance to osteoclasts from normal subjects. IFN-gamma stimulation increased the intensity of TRAP staining (p < 0.0001) to levels near that of the normal osteoclasts. Unstimulated osteoclasts from 6 OP patients had a significantly lower baseline level of superoxide production, as measured by nitroblue tetrazolium reduction (p < 0.0001), compared with normal osteoclasts. IFN-gamma markedly increased (p < 0.0001) superoxide production. Whereas there was a 3-fold increase in superoxide generation in OP patients' osteoclasts, osteoclasts from control subjects had only a small and insignificant increase in superoxide production after IFN-gamma treatment.

Immunoreactivity of peptides generated by limited proteolysis of 71-kDa cell wall protein of Mycobacterium tuberculosis H37Ra using PLG-microparticles.

Peptide mapping by limited proteolysis of a highly protective 71-kDa cell wall-associated protein of Mycobacterium tuberculosis H37Ra was carried out in order to identify key protective determinants within the native protein. The 71-kDa protein, which had an isoelectric point of 4.25, was digested into eight major bands at 48 h using trypsin and pepsin at equal enzyme to protein ratios (pH 5.5). The in vitro lymphocyte reactivity of individual peptides suggested P1, P2 and P5 to be significantly immunoreactive in mice immunized with native 71-kDa-polylactide-coglyeolide (PLG); however, the reactivity was significantly lower than that of the native 71-kDa protein. Immunization of mice with a pooled fraction (upper fraction-71 kDa) of more immunoreactive peptides (consisting of P1 and P2) did not further boost their immunoreactivity. However, P1 and P2 exhibited comparable or even higher lymphocyte proliferation in human tuberculous and control subjects. These data suggest distinct antigenic specificities in humans and mice and further substantiate the use of the 71-kDa protein or its peptides P1 and P2 as potential vaccine candidates for tuberculosis.

Circulating levels of glucagon-like peptide-2 in human subjects with inflammatory bowel disease.

Glucagon-like peptide-2 (GLP-2) is a recently characterized intestine-derived peptide that exerts trophic activity in the small and large intestine. Whether circulating levels of GLP-2 are perturbed in the setting of human inflammatory bowel disease (IBD) remains unknown. The circulating levels of bioactive GLP-2-(1-33) compared with its degradation product GLP-2-(3-33) were assessed using a combination of RIA and HPLC in normal and immunocompromised control human subjects and patients hospitalized for IBD. The activity of the enzyme dipeptidyl peptidase IV (DP IV), a key determinant of GLP-2-(1-33) degradation was also assessed in the plasma of normal controls and subjects with IBD. The circulating levels of bioactive GLP-2-(1-33) were increased in patients with either ulcerative colitis (UC) or Crohn's Disease (CD; to 229 +/- 65 and 317 +/- 89%, P < 0.05, of normal, respectively). Furthermore, the proportion of total immunoreactivity represented by intact GLP-2-(1-33), compared with GLP-2-(3-33), was increased from 43 +/- 3% in normal healthy controls to 61 +/- 6% (P < 0.01) and 59 +/- 2% (P < 0.01) in patients with UC and CD, respectively. The relative activity of plasma DP IV was significantly reduced in subjects with IBD compared with normal subjects (1.4 +/- 0.3 vs. 5.0 +/- 1.1 mU/ml, respectively; P < 0.05). These results suggest that patients with active IBD may undergo an adaptive response to intestinal injury by increasing the circulating levels of bioactive GLP-2-(1-33), facilitating enhanced repair of the intestinal mucosal epithelium in vivo.

Ventricular myocardium in control and growth-retarded human fetuses: Growth in different tissue compartments and variation with fetal weight, gestational age, and ventricle size

The aim of this study was to assess the growth of different tissue compartments in ventricular myocardium of control and intrauterine growth-retarded (IUGR) human subjects. Stereological counting and sizing methods were applied to cross-sectional samples of hearts collected post mortem at 16 to 35 (control) and 32 to 42 (IUGR) gestational weeks. Total tissue volumes and total numbers of myocyte, connective tissue, and endothelial cell nuclei were estimated. In control hearts, the volume of each tissue compartment increased linearly over the period of gestation, and this was due to proliferation, because in each case the tissue volume per nucleus remained constant. In IUGR subjects, fetal weight, ventricle volume, myocyte volume, connective tissue volume, and endothelial nuclear number were less than expected for gestational age up to at least 35 weeks. Between this age and 8 postnatal weeks, these variables are predicted to achieve equivalence with values found in control fetuses. Similar deficits were found when variables were related to fetal weight, and it is predicted that equivalence with control values would be reached at weights of between 2.3 and 3.6 kg. No such differences between groups were detected when variables were related to ventricle size. These findings indicate that growth deficits in cardiomyocytes are accompanied, and may be influenced, by developmental delays that involve the intramyocardial interstitium (capillary bed, endothelium, and surrounding connective tissues). The delays and deficits exhibit “catch-up” to control values between 35 weeks and term.

Levels of alpha1-proteinase inhibitor and alpha2-macroglobulin in the tear film of patients with keratoconus.

Levels of alpha1-proteinase inhibitor and alpha2-macroglobulin in the tear film of patients with keratoconus were measured to elucidate their possible roles in the pathogenesis of keratoconus. Tear samples were collected from 15 keratoconus patients and 14 age-similar human control subjects. Levels of alpha1-proteinase inhibitor and alpha2-macroglobulin in each tear sample were quantified and compared between the two groups. Mean values for alpha1-proteinase inhibitor were 101.0+/-35.5 and 106.1+/-41.7 ng/microg protein for the keratoconus and control groups, respectively. The corresponding mean values for alpha2-macroglobulin were 13.5+/-6.8 and 14.8+/-7.5 ng/microg protein. Neither inhibitor showed a statistically significant difference between the keratoconus and control specimens. Subset analysis to evaluate the effects of contact lens wear and the presence of a graft in the fellow eye did not reveal a statistically significant difference. The tear film of patients with keratoconus contains normal levels of protease inhibitors. Therefore, the tear film may not be a source of the reduced inhibitor levels shown in the corneas of patients with keratoconus.

Molecular and Serological Examination of the Relationship of Human Herpesvirus 8 to Multiple Myeloma: orf 26 Sequences in Bone Marrow Stroma Are Not Restricted to Myeloma Patients and Other Regions of the Genome Are Not Detected

Human herpesvirus 8 (HHV-8) genomic sequences were recently detected by polymerase chain reaction (PCR) and in situ hybridization in bone marrow stromal cells grown from multiple myeloma (MM) patients, but not in cells from control subjects (Rettig et al, Science 276:1851, 1997). We sought to confirm these observations in our own group of MM patients (n = 30). DNA was extracted from adherent stromal cells grown under varying conditions and assayed for HHV-8 sequence using PCR to amplify the orf 26 (KS330) sequence (Chang et al,Science 266:1865, 1997), as initially reported. Samples from human control subjects (n = 25) were concurrently extracted and analyzed. After 30 cycles of amplification, we did not detect any positive samples. In a more sensitive nested PCR, samples from 18 of 30 (60%) MM patients were positive, at about the limit of detection, but orf 26 sequence was also amplified from 11 of 25 (44%) human control samples. However, PCR amplification from other regions of the viral genome (orf 72 and orf 75) was uniformly negative for all MM and control samples, despite equivalent sensitivity. Additionally, all sera from MM patients were negative for HHV-8 IgG by immunofluorescence. Our data do not support a role of HHV-8 in the etiology of MM but may suggest the presence of a related (KS330-containing) virus in MM patients and in some control subjects.This is a US government work. There are no restrictions on its use.

Molecular and Serological Examination of the Relationship of Human Herpesvirus 8 to Multiple Myeloma: orf 26 Sequences in Bone Marrow Stroma Are Not Restricted to Myeloma Patients and Other Regions of the Genome Are Not Detected

Human herpesvirus 8 (HHV-8) genomic sequences were recently detected by polymerase chain reaction (PCR) and in situ hybridization in bone marrow stromal cells grown from multiple myeloma (MM) patients, but not in cells from control subjects (Rettig et al, Science 276:1851, 1997). We sought to confirm these observations in our own group of MM patients (n = 30). DNA was extracted from adherent stromal cells grown under varying conditions and assayed for HHV-8 sequence using PCR to amplify the orf 26 (KS330) sequence (Chang et al,Science 266:1865, 1997), as initially reported. Samples from human control subjects (n = 25) were concurrently extracted and analyzed. After 30 cycles of amplification, we did not detect any positive samples. In a more sensitive nested PCR, samples from 18 of 30 (60%) MM patients were positive, at about the limit of detection, but orf 26 sequence was also amplified from 11 of 25 (44%) human control samples. However, PCR amplification from other regions of the viral genome (orf 72 and orf 75) was uniformly negative for all MM and control samples, despite equivalent sensitivity. Additionally, all sera from MM patients were negative for HHV-8 IgG by immunofluorescence. Our data do not support a role of HHV-8 in the etiology of MM but may suggest the presence of a related (KS330-containing) virus in MM patients and in some control subjects.This is a US government work. There are no restrictions on its use.

Regional and cellular expression of the dentatorubral-pallidoluysian atrophy gene in brains of normal and affected individuals.

Dentatorubral-pallidoluysian atrophy is an autosomal dominant neurodegenerative disorder characterized by dementia and spinocerebellar degeneration. Recently, part of the gene responsible for this disorder was cloned containing a CAG repeat, and predominant neuronal expression of the gene was proved only through Northern blot analysis in rats. In this study, we investigated the regional and cellular expression of the dentatorubral-pallidoluysian atrophy gene in the central nervous system of normal and affected humans, as well as in rat brains. In normal control human subjects, the gene messenger RNA was present in all brain regions examined, with the highest levels seen in the cerebellum, hippocampus, substantia nigra, and pontine nuclei. Its expression in the striatum, globus pallidus, and cerebral cortex was intermediate. The gene was expressed predominantly in neurons; a low but significant level of expression was also seen in glial cells. Neurons susceptible to degeneration in dentatorubral-pallidoluysian atrophy did not selectively express high or low levels of its gene messenger RNA. In brains affected by the disorder, the distribution and levels of gene messenger RNA were comparable to those of the normal controls in all the areas. In the rat brains, gene messenger RNA expression was very similar to that in human brain. It was also expressed predominantly in neurons, while low-level expression was observed in glial cells. It is apparent from these results that the presence of expanded trinucleotide repeats in dentatorubral-pallidoluysian atrophy does not result in the absence of its gene messenger RNA expression or in altered patterns or levels of expression.

Evidence that natural autoantibodies against the nerve growth factor (NGF) may be potential carriers of NGF

Nerve growth factor (NGF) was detected by enzyme-linked immunosorbent assay using the monoclonal anti-NGF antibody 27/21 in natural NGF autoantibodies (NGF NA) purified from sera of control human subjects as well as from sera of patients with rheumatoid arthritis, autoimmune thyroiditis and to a lesser degree in patients with systemic lupus erythematosus as well as in NGF NA from the synovial fluid of patients with spondylarthropathies. Our results suggest that NGF NA may be potential carriers of NGF in the circulation.

Specific repression of the preproendothelin-1 gene in intracranial arteriovenous malformations.

Cerebrovascular arteriovenous malformations (AVMs) display abnormal vascular development and dysautoregulation of blood flow. Genetic mechanisms that contribute to the pathogenesis and phenotype of cerebral AVMs are unknown. As a first step in understanding the pathophysiology of AVMs, the authors investigated the hypothesis that endothelial dysfunction-specifically, deregulation of endothelin-1 (ET-1) secretion-contributes to the abnormal vascular phenotype and the lack of hemodynamic autoregulation elaborated by these lesions. Endothelin-1 peptide and preproendothelin-1 (ppET1) messenger RNA were not detected in the intranidal vasculature of all 17 patients with AVMs studied, but were prominently expressed in human control subjects with normal cerebrovasculature (p < 0.01). Although AVM vasculature lacked ET-1, its expression was prominent in vasculature distant from these lesions, suggesting local repression of the ppET-1 gene. Local repression of ET-1 was specific to AVMs; ET-1 in vascular malformations of patients with Sturge-Weber disease was actually elevated compared to normal controls (p < 0.01). Repression of the ppET-1 gene was an intrinsic phenotype of AVM endothelial cells and was not due to factors in the AVM microenvironment. The authors also showed that ETA receptor expression was low in AVM vasculature compared to normal controls. Together, these results demonstrate that the ppET-1 gene is locally repressed in AVM lesions and suggest a role for abnormal ppET-1 gene regulation in the pathogenesis and clinical sequelae of cerebral AVMs.

Calcineurin (phosphatase 2B) is Present in Neurons Containing Neurofibrillary Tangles and in a Subset of Senile Plaques in Alzheimer's Disease

The accumulation of hyperphosphorylated tau species in neurons in Alzheimer's disease (AD) might result from a relative decrease in their content of protein phosphatases. In this study we have investigated the immunocytochemical distribution of calcineurin (phosphatase 2B) in the hippocampus and temporal cortex of human control subjects and in AD. Calcineurin was strongly expressed in neuronal perikarya and dendrites but only weakly in white matter tracts, both in controls and in AD. The distribution of calcineurin was preserved in AD. By double-immunolabelling with calcineurin antibodies and the AT8 antibody to paired helical filament-tau, it was observed that a strong calcineurin immunoreactivity was still present in many neurons containing neurofibrillary tangles (NFT). Calcineurin was present in dystrophic neurites in some senile plaques (SP) located in the hippocampal formation but more rarely in neocortical areas; this calcineurin immunoreactivity did not always overlap with the tau immunoreactivity in SP. These results suggest that development of NFT in most neurons does not result from a major decrease of calcineurin expression.

Natural autoantibodies against the nerve growth factor in autoimmune diseases

High titers of natural autoantibodies against the nerve growth factor (NGF) were detected in the sera of patients with systemic lupus erythematosus, autoimmune thyroiditis and rheumatoid. Autoantibodies to NGF from these pathological cases displayed higher avidity for NGF and a higher polyreactivity with certain cytoskeletal proteins and with DNA as compared to those from control human subjects. The biological activity, immunoglobulin composition and physiological relevance of these autoantibodies are discussed.

Distensibility of small pulmonary blood vessels.

Although vasomotor activity in small pulmonary vessels has been studied extensively in the past, using the concept of resistance to flow, information on the distensibility of these vessels is very sparse. In an attempt to reduce this deficit, we adapted a theoretical method developed for small systemic vessels, to estimate distensibility of pulmonary resistance vessels in experimental animals and man. Pressure-flow data from 11 dogs and 10 human subjects (5 control subjects and 5 patients with long-standing left heart failure) were used to calculate distensibility of small pulmonary vessels. The conductance, G, was calculated from these data as the ratio of blood flow to driving pressure. The slope of the relationship between the logarithm of G1/4 and the average distending pressure (ADP) provides a graphic picture of circumferential extensibility, E, defined as percent change in radius for an infinitesimal change in ADP. Results indicate that: (1) the value of E in dogs was 1.85 +/- .40 mmHg-1 for the control state, which decreased to 1.45 +/- .43 mmHg-1 during norepinephrine administration; however, the decrease in the value was not statistically significant (p = 0.53); (2) the value of E in control human subjects was 3.38 +/- .47 mmHg-1 and the value of E in patients with left heart failure was -0.64 +/- 0.39 mmHg-1; the difference was significant (P = .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

The assay of S-D-lactoylglutathione in biological systems.

A procedure for the assay of S-D-lactoylglutathione, the physiological intermediate of the glyoxalase system, in biological systems is described, together with sample storage, sample processing, and statistical evaluation. Specimen data are presented. S-D-Lactoylglutathione was assayed by reverse-phase high-performance liquid chromatography (HPLC) with spectrophotometric detection of the thiolester chromophore at 233 nm. The biological sample was deproteinized with perchloric acid and partially purified by strong anion-exchange solid-phase extraction prior to HPLC. The limit of detection was 3.7 nmol, the recovery 49 ± 4%, and the intra- and interbatch coefficients of variance 0.7 and 12%, respectively. The concentration of S-D-lactoylglutathione in whole blood from normal control human subjects was (mean ± SD, nmol/ml whole blood) 16.5 ± 4.4 (n = 8), and from diabetic patients 21.2 ± 9.2 (n = 25), which is a significant increase (P < 0.05) from normal controls. The assay of S-D-lactoylglutathione is of increasing interest in studies of the elevation of glyoxalase metabolites in diabetes mellitus and in investigations of the antiproliferative activity of S-D-lactoylglutathione.

The Assay of S-D-Lactoylglutathione in Biological Systems

A procedure for the assay of S-D-lactoylglutathione, the physiological intermediate of the glyoxalase system, in biological systems is described, together with sample storage, sample processing, and statistical evaluation. Specimen data are presented. S-D-Lactoylglutathione was assayed by reverse-phase high-performance liquid chromatography (HPLC) with spectrophotometric detection of the thiolester chromophore at 233 nm. The biological sample was deproteinized with perchloric acid and partially purified by strong anion-exchange solid-phase extraction prior to HPLC. The limit of detection was 3.7 nmol, the recovery 49 ± 4%, and the intra- and interbatch coefficients of variance 0.7 and 12%, respectively. The concentration of S-D-lactoylglutathione in whole blood from normal control human subjects was (mean ± SD, nmol/ml whole blood) 16.5 ± 4.4 ( n = 8), and from diabetic patients 21.2 ± 9.2 ( n = 25), which is a significant increase ( P < 0.05) from normal controls. The assay of S-D-lactoylglutathione is of increasing interest in studies of the elevation of glyoxalase metabolites in diabetes mellitus and in investigations of the antiproliferative activity of S-D-lactoylglutathione.

Is n-Pentane Really an Index of Lipid Peroxidation in Humans and Animals? A Methodological Reevaluation

Volatile hydrocarbons such as ethane and n-pentane are known to originate from peroxidation of polyunsaturated fatty acids in membrane lipids and they are accepted as a sensitive and direct index of lipid peroxidation both in vitro and in vivo. Until now, an appropriate and commonly accepted method for the analysis of volatile hydrocarbons in exhalation air has not been described. We therefore developed a methodology for routine application in humans that is based on cryofocusing in combination with gas chromatography and is adaptable to mass spectrometry. The samples may be stored in stainless steel bombs up to 3 weeks, and sample volumes necessary to analysis are variable and can be adapted to analytical requirements. The interference by water and carbon dioxide, always present in excess, is strongly reduced. Mass spectroscopic analysis of exhalation air in human control subjects demonstrates, however, the presence of isoprene as the major constituent hitherto identified as n-pentane. The commonly used columns fail to separate n-pentane and isoprene. Based upon studies of the diverse methodologies reported in literature, it must be assumed that the reported responses of the gas chromatographic "n-pentane" peak in exhalation air of humans and animals, hitherto identified exclusively by authentic reference gases, are actually responses to isoprene or, at least, a mixture of both n-pentane and isoprene.

Nicotine blocks latent inhibition in rats: evidence for a critical role of increased functional activity of dopamine in the mesolimbic system at conditioning rather than pre-exposure

Latent inhibition (LI) is a cognitive process whereby repeated exposure of a stimulus without consequence impedes the formation of subsequent associations with that stimulus. A number of studies in the rat have reported that LI is impaired by moderate systemic doses of amphetamine, an effect believed to be mediated via dopamine (DA) release in the nucleus accumbens. We and others have reported that nicotine has a selective effect in releasing DA in the accumbens rather than the caudate nucleus. We have therefore examined the ability of nicotine to disrupt LI, using a conditioned emotional response paradigm. Pre-exposure of a tone stimulus impaired subsequent conditioning between that stimulus and mild footshock, as indexed by suppression of licking by the tone subsequently presented alone. This LI effect was prevented, by an effect confined to the pre-exposed group, by doses of 0.4 or 0.6 mg/kg nicotine SC, which are accumbens selective, given before pre-exposure and before conditioning. The effect of nicotine in disrupting LI was prevented by prior administration of haloperidol at a dose (0.5 mg/kg) reported to reverse the disruptive effect of amphetamine on LI. Although the amphetamine effect requires two administrations, the effect of two administrations of nicotine was reproduced by a single dose of nicotine given before conditioning, but not by a single dose before pre-exposure. The results are discussed in relation to studies in human control and schizophrenic subjects, which suggest that increased DA activity in humans is also associated with impaired LI.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of human growth hormone (GH)-binding protein in human serum on GH binding to rabbit liver membranes

The sequence identity of growth hormone-binding protein (GH-BP) with the extracellular domain of GH receptors raised the possibility that circulating GH-BP might affect the binding of human GH (hGH) to its receptors, and thus, its biological effects. To test this hypothesis, we tested the effects of sera with low GH-BP levels (obtained from prepubertal children, girls with anorexia nervosa [AN], and patients with hepatic cirrhosis), normal control sera, and sera with high GH-BP levels (obtained from obese patients) on hGH binding to its receptors. GH-BP activity in patients' sera was measured by incubation with [ 125I]hGH and the separation of bound hGH from free hGH with dextran-coated charcoal. The effect of GH-BP was studied by preincubation of patients' sera with increasing concentrations of hGH, followed by incubation with [ 125I]hGH and a rabbit liver membrane preparation known to be rich in GH receptors, and finally by measuring hGH bound to the receptors. In this study, we report on the ability of GH-BP to reduce the inhibitory capacity (IC 50) of hGH on [ 125I]hGH binding to GH receptors. The concentration of GH-BP in serum is positively correlated with the IC 50 of hGH incubated with different sera on [ 125I]hGH binding to its receptors (n = 21; r = .886, P < .001). In the presence of high serum GH-BP levels, such as those observed in obesity ( 20.13% ± 0.71% 0.05mL serum), the IC 50 values were significantly higher than those obtained with sera containing GH-BP levels lower than those measured in human control subjects, such as from prepubertal children, AN patients, and cirrhotic patients. Based on these findings, it is proposed that increasing levels of GH-BP may modulate GH binding to its receptor, and thus may exert a negative feedback on receptor recycling and synthesis and on GH-BP cleavage from the membrane receptor or its independent expression.

On the stability of messenger RNA and ribosomal RNA in the brains of control human subjects and patients with Alzheimer's disease.

The levels of the mRNAs encoding the G protein subunits GS alpha, G beta 1, and G beta 2 were measured by northern blotting in the frontal cortex and hippocampus of control subjects and of patients with a clinical and histopathological diagnosis of dementia of the Alzheimer type (DAT). There was no significant difference, in either brain region, between the control and DAT groups for any of the G protein mRNAs measured. The degree of intersubject variability was very high, e.g., GS alpha mRNA in the frontal cortex (mean optical density +/- SD) was 405 +/- 342 in the control group versus 305 +/- 207 in the DAT group. The extent of generalised RNA degradation was assessed by detecting the breakdown products of 28S rRNA. RNA degradation was present in tissue samples from every human subject studied. The extent of 28S rRNA degradation in each subject was found to be related to the levels of G protein mRNA detected. The degree of RNA degradation in human subjects was found to be very variable and unaffected by the presence of DAT. RNA degradation correlated poorly with postmortem interval and this was confirmed by a controlled study of postmortem degradation in rat tissue. The possibility that the relative hypoxia and ischaemia in patients immediately before death could influence RNA degradation is discussed. The variable extent of RNA degradation means that great care must be taken to ensure the validity of RNA analyses undertaken in human postmortem brain, particularly when techniques are employed (such as in situ hybridisation) that themselves give no indication of RNA integrity.

Plasma vitamins A and E and hydrogen peroxide-induced in vitro erythrocyte haemolysis in common marmosets (Callithrix jacchus).

Plasma total lipid, cholesterol, all-trans retinol (vitamin A) and alpha-tocopherol (vitamin E) concentrations, and the susceptibility of erythrocytes to hydrogen peroxide-induced haemolysis in vitro were investigated in healthy laboratory-bred common marmosets (Callithrix jacchus). The concentrations of alpha-tocopherol and total cholesterol were similar to those of control human subjects. The mean lipid concentration was higher (P less than 0.025) and the retinol concentration lower (P less than 0.001) in the marmosets. The susceptibility of the erythrocytes of the marmosets to hydrogen peroxide-induced haemolysis was high, both in absolute value and relative to the controls. Changes in phospholipid and fatty acid composition might have rendered the red cells susceptible to oxidative stress.