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PubMed1983

Subsets of blood, spleen and recirculating lymphocytes in man.

Lymphocyte subpopulations were characterized in human blood and spleens. In addition the spleens were perfused by a closed extracorporeal perfusion system under almost physiological conditions. Lymphocytes released from the spleen during perfusion were taken to be representative of recirculating lymphocytes. B lymphocytes were classified by their surface immunoglobulin, T lymphocytes and T lymphocyte subsets by cytochemistry, sheep red blood cell rosette formation and in some experiments by monoclonal antibodies. In the blood 71 +/- 4.3% of the lymphocytes were rosette forming cells and 23.3 +/- 3.8% B lymphocytes. In the spleen 49.8 +/- 3.6% were T and 53.3 +/- 2.1% were B lymphocytes. In three spleens the mean number of OKT3+ lymphocytes were 27.6 +/- 7.0% OKT4+ 8.6 +/- 1.4% and OKT8+ 13.7 +/- 2.2%. The ratio of T helper to T suppressor lymphocytes was 0.67 for the spleen and 1.7 for the blood. The lymphocytes released from the perfused spleen showed a similar distribution pattern of surface markers to that of the splenic subpopulations.

Aged↗
PubMed1981

Adherent spleen cells from mice acutely infected with cytomegalovirus suppress the primary antibody response in vitro.

In the present study, we have demonstrated that the hemolytic plaque response of spleen cells from mice acutely infected with murine cytomegalovirus (MCMV) is suppressed in vitro. Mishell-Dutton cultures established with spleen cells from C57BL/6 mice infected 4 days earlier with 4.2 X 10(3) plaque-forming units of MCMV were found to produce significantly fewer direct plaques upon stimulation with sheep red blood cells than corresponding control cultures. Suppression could not be attributed to a generalized lytic destruction of spleen cells, nor was it produced by addition of virus directly to uninfected spleen cell cultures. However, in cultures containing various mixtures of cells from control and infected mice, the direct plaque response was markedly below the predicted response, suggesting that the uninfected cells were actively suppressed by cells from infected mice. Suppression was dependent on the presence of intact spleen cells, since it was not found in the presence of lysed cells. The capacity of spleen cells from infected mice to mediate suppression was demonstrated in the plastic-adherent subpopulation. Treatment of these cells with anti-thymocyte serum (ATS) and complement did not abolish the capacity to suppress the immune response. Thus, adherent ATS-resistant cells from the spleens of mice acutely infected with MCMV, rather than virus alone, have the capacity to actively suppress the hemolytic plaque response in vitro.

Animals↗
PubMed1980

Tumor-specific suppressor cells induced by immunization with spleen cells from tumor-bearing animals.

Spleen cells from Fischer rats immunized with syngeneic spleen cells immune to the syngeneic 13762A mammary adenocarcinoma inhibited in vitro generation of lymphocytes cytolytic to the tumor. Spleen cells from rats immunized with nonimmune spleen cells were not suppressive. The suppressive property was first detected 10 days after immunization, persisted through the 17th day, and generally correlated with the appearance of an immunoglobulin G (IgG) factor blocking cell-mediated cytotoxicity to the tumor. Suppression was mediated chiefly by T-lymphocytes, but IgG-bearing lymphocytes also had some suppressive ability. Suppression was induced by IgG-positive cells or by serum or IgG from rats immunized to the 13762A mammary adenocarcinoma. The suppressor cells in the spleens of serum-immunized rats appeared earlier (3 days) than after immunization with immune spleen cells (10 days). These results suggest that certain IgG-positive spleen cells, as well as IgG present in the same tumor-bearing animals, induce one type of suppressor cell modulating cytolytic lymphocyte activity to this mammary adenocarcinoma.

Adenocarcinoma↗
PubMed1984

Tc-99m diphosphonate and sulfur colloid uptake by the spleen in sickle disease: interrelationship and clinical correlates: concise communication.

To determine the clinical significance of splenic uptake in bone scintigraphy and functional asplenia on the radionuclide liver-spleen image, bone and spleen scintigrams of 38 patients with sickle cell disease were reviewed. Eighteen underwent bone and liver-spleen studies, 15 had only bone images, and five had only liver-spleen studies. Sixteen of 33 who had bone scintigraphy showed splenic uptake, but the frequency of homozygous sickle cell (SS) disease was not greater than heterozygous sickle cell disease (S-hetero) in this group. SS patients with splenic uptake of Tc-99m diphosphonate had significantly fewer painful crises of the abdomen and extremities, and fewer inpatient and outpatient hospital visits than SS patients whose bone imaging did not visualize the spleen. Functional asplenia on liver-spleen images (16 cases) was seen only in SS disease. One SS patient, age 8, still had a spleen capable of phagocytizing colloid.

Adolescent↗
PubMed1982

Spleen cell transfer induces T cell-dependent granulomas in tuberculous nude mice.

After IV infection with an attenuated strain of Mycobacterium bovis BCG, athymic nude mice produced a few hepatic granulomas; most of the other foci of bacterial parasitization lacked obvious cellular reactions. Nude mice BCG-infected four weeks earlier received spleen cells from normal euthymic littermates. After transient splenomegaly which peaked at about two weeks, numerous hepatic granulomas appeared by four weeks and the number of viable BCG decreased. The development of hepatic granulomas required viable spleen cells and depended on the spleen cell dose and corresponded with positive footpad reactions. The effective population seemed to be T cells, since they were sensitive to treatment with anti-brain associated theta antigen serum (antiBAT) plus complement, and were found in nylon-wool passed fractions. After transfer with sensitized spleen cells, adoptive immunity was observed, provided that the recipient BCG-infected nude mice had been splenectomized before transfer. AntiBAT plus complement treatment of the sensitized spleen cells decreased the granuloma-producing as well as antimycobacterial capacity. When BCG-infected nude mice were irradiated with 500 r of gamma ray, granuloma production was decreased after immune spleen cell transfer. Co-transfer of immune spleen cells with normal nude mouse bone marrow cells to BCG-infected irradiated nude recipients restored the granuloma-forming ability.

Animals↗
PubMed1978

In vitro activation of suppressor cells from spleens of mice treated with radioactive strontium.

Mice were treated with two 100-muCi injections of 89Sr to deplete marrow-dependent (M) cells. Mice so treated responded normally to immunization with sheep red blood cells (SRBC) in vivo; moreover, spleen cells from 89Sr-treated mice were able to respond to SRBC after infusion into irradiated recipient mice. However, spleen cells from mice treated with 89Sr did not respond to SRBC in vitro and mixtures of normal spleen cells with the latter were also not able to respond in vitro. The discrepancy between in vivo and in vitro responses was abolished by culturing spleen cells for 24 hr before testing their ability to respond to SRBC in the adoptive transfer in vivo. Pretreatment of spleen cells from 89Sr-treated mice with 1000 R of gamma-radiation lessened their suppressive activity. The suppressor cells were detected in spleens of athymic nude mice treated with 89Sr. The suppressive activity, after the 24-hr culture period, was not abolished by irradiation and was active in vivo as well as in vitro. Thus, depletion of M cells by 89Sr results in the appearance within the spleen of thymus-independent suppressor cells, which require a short period of in vitro cultivation before becoming functionally active.

Animals↗
PubMed1981

Modulation by serum from irradiated and marrow transplanted mice of hemopoietic regeneration in mouse spleen organ cultures.

A spleen organ culture system has been used to analyse hemopoietic progenitor cell (CFC) regeneration in the C57BL mouse spleen following 800 rad whole-body irradiation and the injection of 10(7) syngeneic bone marrow cells. The linear regeneration pattern observed in vitro compared to an initial decrease followed by a rapid increase in CFC levels in vivo suggested a possible modulating influence of humoral factors in vivo on hemopoietic regeneration in the spleen. In agreement with this, addition of mouse serum collected at various time intervals after irradiation and transplantation to spleen organ cultures in vitro was able to reproduce accurately the kinetics of CFC regeneration seen in spleens in vivo. In addition the possible role played by colony stimulating factors (CSF) in the regulation of CFC regeneration in spleen organ cultures was investigated. No clear evidence was found for the importance of CSF in regulating the CFC regeneration in organ cultured spleens.

Animals↗
PubMed1982

The relative roles of the spleen and bone marrow in platelet production in mice.

The relative importance of the spleen and bone marrow in platelet production is not known. In an attempt to delineate these roles in mice, the spleen was removed by surgical excision or the bone marrow was ablated with an injection of strontium-89 (89Sr). Platelet production in these mice was compared with that in untreated mice, 88Sr (nonradioactive strontium)-treated mice, sham-splenectomized mice, and whole-body irradiated mice. Platelet production, platelet counts, and platelet sizes were similar in strontium-89 marrow-ablated mice and whole-body irradiated mice, as were RBC counts, WBC counts and hematocrit values, until the spleens of the 89Sr-treated mice became larger (150% of normal by day 9) and apparently began to produce platelets to compensate for the thrombocytopenia that resulted from the loss of the bone marrow. Splenectomy did not affect the ability of mice to maintain normal platelet production and platelet counts, or RBC counts, WBC counts, and hematocrit values. Therefore, under normal conditions the spleen appears to contribute little or nothing to platelet production in mice, but after bone marrow removal, platelet production by the spleen may occur as a compensatory mechanism. The platelets produced by the compensating spleen resemble in size those platelets that are normally produced by the marrow after thrombocytopenia, with above average sizes. After splenectomy, platelets were were smaller than normal indicating that older, smaller platelets were being retained in the circulation; loss of the spleen could also cause a temporary deregulation of the bone marrow resulting in the production of small platelets.

Animals↗
PubMed1982

Effects of BCG and cyclophosphamide on the spontaneous and antibody-dependent cell-mediated cytotoxicity of peritoneal and spleen lymphocytes of ACI/N rats.

The effects of BCG and cyclophosphamide on the antibody-dependent cell-mediated cytotoxicity (ADCC) and natural killer (NK) activity of spleen and peritoneal lymphocytes were serially examined after treatment. The changes of ADCC and NK activity were different in peritoneal and spleen lymphocytes according to the route and timing of administration. The decrease of NK activity induced by cyclophosphamide is not marked, and the degree of decrease depends on the timing of cyclophosphamide administration. The ADCC and NK activity of peritoneal lymphocytes after intravenous BCG administration were elevated 7 days after treatment, but the NK activity of spleen lymphocytes was decreased. On the other hand, the NK activities of peritoneal and spleen lymphocytes were elevated in rats given intraperitoneal BCG. Spleen lymphocytes and peritoneal lymphocytes from rats given intravenous BCG suppressed tumor growth in the Winn test during the early tumor-bearing stage. The spleen lymphocytes with low NK activity in rats given intravenous BCG strongly suppressed the NK activity of normal spleen lymphocytes.

Animals↗
PubMed1982

Effects of the spleen, epinephrine, and splenectomy on determination of blood volume in cats.

Blood volume (BV), RBC mass, plasma protein (PP), and PCV were determined in (i) awake, nonsplenectomized (NSPX) cats before and after splenic contraction was induced by IV administration of epinephrine, (ii) in pentobarbital-anesthetized, NSPX cats before and after splenic contraction was induced by epinephrine and splenectomy, and (iii) in awake, splenectomized (SPX) cats before and after epinephrine was administered. Blood volume, absolute RBC mass in the spleen could not be determined accurately in awake or anesthetized, NSPX cats. Accurate BV and RBC mass determinations could only be obtained in cats without the spleen; mean BV and RBC mass of awake or anesthetized, SPX cats were 4.1% and 1.4% or body weight, respectively. The spleen was a dynamic sequestering organ for feline erythrocytes (RBC). Epinephrine (0.1 ml of 1:1,000) given IV resulted in the observed contraction of the spleen within 2 minutes. Relaxation of the spleen with RBC uptake began 3 minutes after epinephrine was given and it proceeded at a rate of approximately 0.93% of circulating PCV/min. At 20 minutes after epinephrine was given, a steady state of PCV occurred, and 20% of the maximum circulating PCV observed after the administration of epinephrine was stored within the spleen. At 60 minutes after epinephrine was given to awake, SPX cats, intravascular fluid influx of 4 ml/kg resulted in a decrease of PCV and PP. At 3 hours after splenectomy was done, intravascular fluid efflux resulted in hemoconcentration--a calculated fluid deficit of 2.5 ml/kg/hr occurring during the 3 hours after surgical removal of the spleen.

Anesthesia, General↗
PubMed1975

Dynamics of thymidine incorporation by spleen cells from rats infected with Plasmodium berghei.

The in vitro incorporation of thymidine by spleen cells of rat infected with Plasmodium berghei was higher than that of normal rat spleen cells. The incorporation was proportional to the number of cells in the system and was related to the day of infection, e.g. spleen cells from malarious rats incorporated up to forty times as much thymidine as did normal spleen cells 21 days after inoculation. At the same time, the response of the malarious spleen cells to phytohaemagglutinin (PHA) was only one-twentieth of that observed for normal spleen cells. The thymidine was incorporated by non-adherent spleen cells in a single pulse during the first 8 hr in culture.

Animals↗
PubMed1976

Human spleen heme oxygenase in normal, hemolytic and other pathological states.

Heme oxygenase (HO), the primary enzyme responsible for heme catabolism, was measured in spleens from 10 normal subjects, 14 patients with chronic hemolytic anemia (HA), 12 with idiopathic thrombocytopenic purpura (ITP), and 10 with various lymphoproliferative disorders (LD) to determine the splenic enzymatic capacity for heme catabolism and the response of splenic HO to hemolysis. Splenic NADPH-cytochrome c reductase activity and cytochrome P-450 levels were also measured. Splenic HO specific activity in normal spleens was 0.235 +/- 0.106 (SE) nmoles bilirubin/mg protein/min; in HA, 0.276 +/- 0.050; in ITP, 0.228 +/- 0.036; and in LD, 0.420 +/- 0.105. However, the total HO activity per spleen was significantly greater in HA (742.9 +/- 137.4 (SE) nmoles/min, p less than 0.001) and LD (681.9 +/- 180.3, p less than 0.005) than in normal spleens (137.1 +/- 55.0), but was not significantly increased in ITP (269.5 +/- 121.5). In normal spleens cytochrome P-450 was 0.052 +/- 0.006 (SE) nmoles/mg and NADPH-cytochrome c reductase activity was 8.3 +/- 2.2 (SE) nmoles/mg/min; neither of these specific activities was significantly altered in HA, ITP, or LD. Again, total activity was significantly increased in HA and LD associated with increased splenic size. Although total HO activity is greater in the larger spleens, HO activity does not increase per unit weight of tissue. In normal spleen the calculated capacity for bilirubin production by HO was 115 mg per day. This accounts for only 50% of normal daily production from erythroid sources and suggests that other sites are of major importance for hemoglobin degradation.

Anemia, Hemolytic↗
PubMed1993

Characterization of ferritin from spleens of patients with Hodgkin's disease (HD).

Ferritin, an iron-storing protein, was isolated from disease-involved and -uninvolved regions of spleen biopsies obtained from patients with Hodgkin's disease (HD). Ferritin from all human spleen biopsies showed a major band of polypeptide of M(r) around 20 kDa in 1D-SDS-PAGE analysis. The corresponding bands for horse spleen ferritin and apoferritin (Sigma) were at a slightly lower M(r) level. In isoelectrofocusing (IEF) studies, the pI values of human spleen ferritin from the uninvolved and involved regions were 4.55 and 4.14, respectively. These were more acidic than that of horse spleen ferritin (4.79). Human spleen ferritin from the involved region also differed from that of the uninvolved region in the pattern of CNBr-generated peptide maps in 1D-SDS-PAGE. These results suggest that the presence of Hodgkin's disease in human spleen is associated with some physiochemical changes in the tissue ferritin.

Animals↗
PubMed1977

Production of thymic cells by mouse spleen and bone marrow.

Karyotype difference between the AKR/TIALD strain (T1) that bears 2 metacentric markers, and the AKR strain (no marker) was used to follow the thymic repopulation of lethally irradiated (AKR X T1) F1 hybrids restored by AKR bone marrow (BM) or spleen cells. Eleven days following radiation exposure, 40-50% of the thymic cells were BM-derived in the mice restored with BM cells whereas spleen-derived cells remained below 10% in those restored with spleen cells. The thymic repopulation by spleen-derived elements was enhanced either by injecting a larger munber of spleen cells or by adding thymic cells to the spleen inoculum; however in both cases the appearance of the spleen-derived karyotypes still required a delay of about 11 days. The thymic cells could either recruit thymic precursor cells or trigger their multiplication. On the opposite, it has not been possible to demonstrate a favorable effect of the injected thymic cells on the repopulation of the thymus by BM-derived elements.

Animals↗
PubMed1996

Interaction of stem cell factor and its receptor c-kit mediates lodgment and acute expansion of hematopoietic cells in the murine spleen.

The phenotypes of mice that harbor a defect in the genes encoding either stem cell factor (SCF) or its receptor, c-kit, indicate that this ligand/receptor pair is necessary for maintenance of normal hematopoiesis in the adult. Our objective was to determine whether SCF, like erythropoietin, is necessary for acute erythroid expansion during recovery from hemolytic anemia. Monoclonal antibody ACK2, which recognizes the murine c-kit receptor, was used to selectively block the hematopoietic growth-promoting effects of SCF. Mice were treated with phenylhydrazine on day 0 and day 1 to induce hemolytic anemia and also received no antibody, control IgG, or ACK2 on day 0. The mice were killed on day 3 and the hematocrit (Hct), reticulocyte count, and numbers of erythroid and myeloid hematopoietic progenitor cells (colony-forming unit-erythroid [CFU-E], burst-forming unit [BFU]-E, and CFU-granulocyte-macrophage [GM]) were quantitated in the femoral marrow and spleen using hematopoietic colony-forming assays. Induction of hemolytic anemia with phenylhydrazine resulted in a drop in the Hct from approximately 50% to 30%, and an approximate 8- to 10-fold increase in the reticulocyte count. The numbers of CFU-E increased modestly in the femur, and approximately 25- to 50-fold in the spleen, in comparison with normal mice. BFU-E and CFU-GM values did not increase in the femur but expanded 6- to 10-fold in the spleen, in comparison with normal mice. This confirms that much of the erythroid expansion in response to hemolytic anemia occurs in the murine spleen. Neutralizing quantities of the ACK2 antibody reduced femoral CFU-E, BFU-E, and CFU-GM content to less than half that found in phenylhydrazine-treated control mice and nearly totally ablated splenic hematopoiesis. These results suggest that c-kit receptor function may be required for optimal response to acute erythropoietic demand and that erythropoiesis in the splenic microenvironment is more dependent on SCF/c-kit receptor interaction than is erythropoiesis in the marrow microenvironment. Because expansion of late erythropoiesis in the spleen was preferentially blocked, we tested the hypothesis that homing of more primitive hematopoietic cells to the spleen was dependent on c-kit receptor function. Lethally irradiated mice were injected with marrow cells obtained from mice that had received phenylhydrazine plus control IgG or with marrow cells obtained from mice that had received phenylhydrazine plus ACK2. In parallel experiments, normal murine marrow cells were treated in vitro with control IgG or with ACK2 and were injected into lethally irradiated mice. The fraction of BFU-E and CFU-GM retrieved from the marrow and spleen of the recipient mice 4 hours later was reduced by approximately 75% when progenitor cells had been exposed to ACK2, in comparison with control IgG. These data suggest that interaction of SCF with the c-kit receptor affects the homing behavior of hematopoietic progenitor cells in the adult animal.

Anemia, Hemolytic↗
PubMed1998

[The characteristics of the development of the immune function in the transplanted spleen of newborn mouse pups in recipients of different ages. 2. The effect of the thymus on the functional development of the transplant].

The effect of the neonatal thymus grafting or "Thymostimulin" administration on the cellularity, cell composition, immune, response to SRBC and proliferative activity of T- and B-cells in vitro were determined in neonatal spleen grafted CBA/Ca female mice of different ages. Analysis of the thymus graft effect on the T- and B-cells content in the spleen transplant from the adult and old recipients demonstrated no differences. The neonatal thymus grafting led to the essential increase of the immune response, spleen cellularity and to the diametrically opposed changing from negative to positive of the sign of the correlation coefficient between the T-cells content and the cellularity of the neonatal spleen in the old recipients. The similar effect of the neonatal thymus grafting was revealed in respect of correlative connection between content of the T-cells and PFCs in spleen grafted to the old recipients too. The "Thymostimulin" injection led only to the increase of the spleen transplant cellularity. These results suggests that the young thymic microenvironment is essential for the normal T-cells differentiation and for its normal function in the neonatal spleen transplant.

Adjuvants, Immunologic↗
PubMed1998

Early morphological and immunological alterations in the spleen during magnesium deficiency in the rat.

Dietary magnesium deficiency in rodents, and especially in rats, causes inflammation and leads to alterations in the immune response. One of the characteristics of magnesium deficiency in the rat is a marked enlargement of the spleen. Considering the importance of the spleen for the immune response, in this study we have evaluated histological, cytological and immunological changes in this organ of rats in early stages of this deficiency. For this purpose, male weaning Wistar rats were pair-fed with either control or magnesium-deficient diet, for 2, 4 or 8 days. Results indicate that after 8 days on the deficient diet rats presented clinical signs of inflammation, splenomegalia and leukocytosis. As shown by histometrical analysis, both the red and white spleen pulps of deficient rats displayed an increased incidence of polymorphonuclear leukocytes and macrophages in all studied stages of deficiency. Concomitantly, the relative number of lymphocytes decreased. This observation was confirmed by the analysis of the cell suspension obtained from the spleen. The greater number of adherent cells in the cell suspension from deficient rats provides an additional confirmation of the increased number of macrophages in the spleen of these rats. Analysis of lymphocyte populations demonstrated a reduced proportion of CD5+ and CD8+ cells after 8 days of deficiency. The reduction in the number of CD8+ cells in deficient rats could be related to the observed decrease in IFN-gamma concentration in the spleen homogenate. In short, this study shows that magnesium deficiency causes early cytological and immunological modifications in the spleen which appeared before macroscopical changes in this organ and before clinical symptoms of inflammation. These changes could be related to the altered immune response of deficient animals.

Animals↗
PubMed2005

Genotoxic activities of aniline and its metabolites and their relationship to the carcinogenicity of aniline in the spleen of rats.

Aniline (in the form of its hydrochloride) has been shown to induce a rather rare spectrum of tumors in the spleen of Fischer 344 rats. The dose levels necessary for this carcinogenic activity were in a range where also massive effects on the blood and non-neoplastic splenotoxicity as a consequence of methemoglobinemia were to be observed. This review aimed at clarifying if aniline itself or one of its metabolites has a genotoxic potential which would explain the occurrence of the spleen tumors in rats as a result of a primary genetic activity. The database for aniline and its metabolites is extremely heterogeneous. With validated assays it ranges from a few limited Ames tests (o- and m-hydroxyacetanilide, phenylhydroxylamine, nitrosobenzene) to a broad range of studies covering all genetic endpoints partly with several studies of the same or different test systems (aniline, p-aminophenol, p-hydroxyacetanilide). This makes a direct comparison rather difficult. In addition, a varying number of results with as yet not validated systems are available for aniline and its metabolites. Most results, especially those with validated and well performed/documented studies, did not indicate a potential of aniline to induce gene mutations. In five different mouse lymphoma tests, where colony sizing was performed only in one test, aniline was positive. If this indicates a peculiar feature of a point mutagenic potential or does represent a part of the clastogenic activity for which there is evidence in vitro as well as in vivo remains to be investigated. There is little evidence for a DNA damaging potential of aniline. The clastogenic activity in vivo is confined to dose levels, which are close to lethality essentially due to hematotoxic effects. The quantitatively most important metabolites for experimental animals as well as for humans (p-aminophenol, p-hydroxyacetanilide) seem to have a potential for inducing chromosomal damage in vitro and, at relatively high dose levels, also in vivo. This could be the explanation for the clastogenic effects that have been observed after high doses/concentrations with aniline. They do not induce gene mutations and there is little evidence for a DNA damaging potential. None of these metabolites revealed a splenotoxic potential comparable to that of aniline in studies with repeated or long-term administration to rats. The genotoxicity database on those metabolites with a demonstrated and marked splenotoxic potential, i.e. phenylhydroxylamine, nitrosobenzene, is unfortunately very limited and does not allow to exclude with certainty primary genotoxic events in the development of spleen tumors. But quite a number of considerations by analogy from other investigations support the conclusion that the effects in the spleen do not develop on a primary genotoxic basis. The weight of evidences suggests that the carcinogenic effects in the spleen of rats are the endstage of a chronic high-dose damage of the blood leading to a massive overload of the spleen with iron, which causes chronic oxidative stress. This conclusion, based essentially on pathomorphological observations, and analogy considerations thereof by previous authors, is herewith reconfirmed under consideration of the more recently reported studies on the genotoxicity of aniline and its metabolites, on biochemical measurements indicating oxidative stress, and on the metabolism of aniline. It is concluded that there is no relationship between the damage to the chromosomes at high, toxic doses of aniline and its major metabolites p-aminophenol/p-hydroxyacetanilide and the aniline-induced spleen tumors in the rat.

Acetaminophen↗