In spleen

Histological changes in the spleen related to diisopropyl methylphosphonate intake were not observed in male or female rats exposed to 1 mg/kg/day of diisopropyl methylphosphonate in their drinking water for 26 weeks (Army 1978). As discussed in Section 2.2.2.1, there is some confusion concerning the concentration units and purity of the diisopropyl methylphosphonate used in the Army (1978) study (EPA 1989), and therefore results from the Army (1978) study are considered inappropriate for human health risk assessment. No changes in spleen weight were noted in male or female mink exposed to... 

Junctions up to 150 nm, basement membrane absent in liver and discontinuous in spleen and bone marrow... 

Recently, it has been shown that inhalation of MWNTs caused suppression of the systemic immunity without resulting in significant lung inflammation or tissue damage [82,83]. Inhaled MWNTs in fact modified the functionality of spleen cells in exposed mice [82]. Notably, the activity of cyclooxygenase (COX) enzymes in spleen was affected as a response to a cytokine (TGF(5) released from the lungs. This cytokine activated the COX pathway in the spleen, triggering T-cell dysfunction and systemic immunosuppression [83]. 

Figure 8.1 Body iron stores and daily iron exchange. The figure shows a schematic representation of the routes of iron movement in normal adult male subjects. The plasma iron pool is about 4 mg (transferrin-bound iron and non-transferrin-bound iron), although the daily turnover is over 30 mg. The iron in parenchymal tissues is largely haem (in muscle) and ferritin/haemosiderin (in hepatic parenchymal cells). Dotted arrows represent iron loss through loss of epithelial cells in the gut or through blood loss. Numbers are in mg/day. Transferrin-Tf haemosiderin - hs MPS - mononuclear phagocytic system, including macrophages in spleen and Kupffer cells in liver.

When lanthanides are injected, even in citrate solutions, with added stable carrier or as low-specific-activity reactor-produced tracers (a) most of the activity, even of those lanthanides that usually deposit in bone, is shunted to liver and spleen (b) in rodents the loss of the liver burden is delayed (c) the deposition in spleen is high and (d) autoradiographs demonstrate reticuloendothelial uptake in liver and spleen (Durbin et al., 1956a Moskalev, 1961b Thomas et al., 1971). 

Treated rats had 1000 mg/kg FW liver (vs. 4.7 in controls) lowered hemoglobin, hematocrit, and red cell counts mean survival time of 67 days hepatic and renal histopathology Dose-time-dependent increase in copper concentrations in liver, spleen, and lung little accumulation in muscle and skin. Reduced growth at 2.5 and 3.75 mg/kg BW daily reduced survival at 3.75 mg/kg BW. Maximum copper concentrations recorded, in mg/kg FW (vs. saline controls,) were 710 in liver (<5), 212 in kidney (<10), 7 in lung (<1.5), 27 in spleen (<2.0) 6 in bone (<2.0) and 2.2 in testes (<1.6) Increased serum ceruloplasmin and white blood cell number... 

Normal spleen lymphocyte function Maximum nickel concentrations in tissues (in mg/kg FW) were reached in blood (19.8) and placentas (3.9) 2 h following injection those in liver (4.9), spleen (1.3), and kidneys (56.2) were reached 4 h after injection and maximum concentration in fetal tissues (1.1) was reached after 8 h. Authors estimate that all nickel is excreted in 42 to 84 h Immunosuppression in spleen lymphocyte function LD50 (48 h)... 

Ewes given oral dose of 74,000 Bq 137Cs, observed for 76 days At 76 days, only 26% of 137Cs remained tissue concentrations, in Bq 137Cs/kg FW, were 77,000 in salivary gland 42,000 in muscle 24.000- 36,000 in pancreas, liver, and kidney 14.000- 17,000 in spleen and lung and <8000 in other tissues 38... 

FIGURE 7.7 (See color insert) Adoptively transferred D011.10 transgenicT cells can be identified by expression of CD4+ and KJ-126 in spleen cell suspension from Balb/c mice after ovalbumin (OVA) immunization. Balb/c mice were injected iv with D011.10 spleen cells containing 3-5 x 1 06CD4+KJ-126+ cells and immunized by intraperitoneal injection of 2 mg OVA emulsified in complete Freund s adjuvant 2 days later. OVA immunization increases the frequency of KJ+T cells and alters the expression of various surface molecules consistent with T cell (Tc) activation. 

Kinser, S. et al. Gene expression profiling in spleens of deoxynivalenol-exposed mice Immediate early genes as primary targets. J. Toxicol. Environ. Health A 67, 1423, 2004. 

Zhou, H. R., Islam Z., and Pestka J.J. Rapid, sequential activation of mitogen-activated protein kinases and transcription factors precedes proinflammatory cytokine mRNA expression in spleens of mice exposed to the trichothecene vomitoxin. Toxicol. Sci. 72,130,2003. 

Pregnant mice exposed to benzene from gestation day 12.5 to 19.5 resulted in the reduction of fetal liver pre-B and B cells. Responsiveness to the B cell mitogen LPS was decreased in spleen cell cultures. The results indicate that in utero exposure to benzene alters fetal lymphopoiesis that may be responsible for compromised immune responsiveness postnatally.104... 

FIGURE 7.7 Adoptively transferred DO11.10 transgenic T cells can be identified by expression of CD4+ and KJ-126 in spleen cell suspension from Balb/c mice after ovalbumin (OVA) immunization. For description, see page 112. 

There was an increased incidence of a mycoplasma respiratory tract infection in rats exposed to 260 ppm hexachloroethane for 6 weeks but not in rats exposed to lower doses or in other species. This could indicate compromised immune function or a weakened mucosal barrier along the respiratory epithelium. There were no studies identified that evaluated a wide range of immunological parameters. Therefore, there are no reliable LOAELs or NOAELs for this end point. Increases in spleen weights are not classified as LOAELs since they were not accompanied by histopathological changes. 

Mercuric chloride in the BN rat gives a lymphoproliferation in spleen and lymph nodes, including B and T helper cells, an increase in the number of Ig containing cells resulting in a rise in all serum Ig isotypes and an early thymic atrophy [196]. The kinetics of the increase in the serum level of various Ig isotypes were similar to that observed for IgE, suggesting spontaneous autoregulation, which could involve suppressor T cells [ 197, 198] and/or auto-anti-idiotypic antibodies [ 199]. 

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