Carbon tetrachloride is immunosuppressive and decreases host resistance to Listeria monocytogenes and Streptococcus pneumoniae in female B6C3F1 mice.
Carbon tetrachloride (CCl(4)) is an environmental contaminant that has been detected in ambient air, seawater, surface-water and snow. The immunotoxic potential of CCl(4) was evaluated in female B6C3F1 mice. The animals were administered with CCl(4) daily for 14 days at doses of 50, 100, 500 or 1000 mg/kg body weight by gavage with corn oil as a vehicle. Exposure to CCl(4) resulted in an increase of liver weight but not the body weight and the weights of brain, spleen, lungs, thymus and kidneys. Exposure to CCl(4) produced minimal effect on differential hematological parameters; however, it produced a significant increase in serum glutamic-pyruvic transaminase (SGPT) levels in all dose groups while other serum chemistries showed sporadic increases, primarily at the dose level of 1000 mg/kg. Exposure to CCl(4) produced a decreased humoral immune response; the IgM antibody forming cell (AFC) response to sheep red blood cells (sRBC) was suppressed with the maximal decrease (45%) observed at the dose level of 1000 mg/kg. The IgM serum titer to sRBC was also reduced with a maximal decrease (54%) observed at the dose level of 500 mg/kg. Although exposure to CCl(4) had no effects on the mixed leukocyte response (MLR), cytotoxic T lymphocyte activity and natural killer (NK) cell activity, a decrease in both the absolute number and the percentage of CD4(+)CD8(-) at the dose level of 500 mg/kg was observed. The functional activity of the mononuclear phagocyte system was compromised as reflected by a decrease in the vascular clearance of (51)Cr-sRBC and a decrease in the uptake of (51)Cr-sRBC by the liver. Finally, in the two host resistance models evaluated, exposure to CCl(4) decreased host resistance to both Streptococcus pneumoniae and Listeria monocytogenes with greater susceptibility to the latter. Overall, these studies demonstrate that CCl(4) was immunosuppressive in female B6C3F1 mice.
Guo
T L
TL
Department of Pharmacology and Toxicology, Virginia Commonwealth University, PO Box 980613, Richmond, VA 23298-0613, USA.
McCay
J A
JA
Brown
R D
RD
Musgrove
D L
DL
Germolec
D R
DR
Butterworth
L
L
Munson
A E
AE
White
K L
KL
D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D002251:Carbon Tetrachloride / Q000276:immunology / Q000633:toxicity*; D002455:Cell Division; D002860:Chromium Radioisotopes / Q000737:chemistry; D004797:Enzyme-Linked Immunosorbent Assay; D004906:Erythrocyte Count; D005260:Female; D005434:Flow Cytometry; D006400:Hematocrit; D006454:Hemoglobins / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D007694:Killer Cells, Natural / Q000276:immunology; D007958:Leukocyte Count; D008089:Listeria monocytogenes / Q000472:pathogenicity*; D008088:Listeriosis / Q000276:immunology*; D016131:Lymphocyte Subsets; D051379:Mice; D009929:Organ Size; D011008:Pneumococcal Infections / Q000276:immunology*; D012588:Scintillation Counting; D013296:Streptococcus pneumoniae / Q000472:pathogenicity*; D010948:Viral Plaque Assay
D002860:Chromium Radioisotopes; D006454:Hemoglobins; D007075:Immunoglobulin M; D002251:Carbon Tetrachloride; D000410:Alanine Transaminase