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The effects of gallium arsenide (GaAs) exposure on immunocompetence of B6C3F1 female mice were investigated. GaAs was administered as a single intratracheal instillation at doses of 50, 100, and 200 mg/kg. Fourteen days after exposure, various cellular and humoral immune parameters were assessed. GaAs exposure increased spleen cellularity in a dose-dependent manner. However, the percentages of Thy 1.2 positive and Ig positive cells were decreased and that of F4/80 positive cells was increased dose dependently. The IgM and IgG antibody-forming cell response of the spleen to the T-dependent antigen sheep erythrocytes was reduced by 66 and 48%, respectively, at 200 mg/kg. Levels of the serum complement protein, C3, were increased by as much as 16% with no significant change in CH50 levels. The mitogenic response of splenic T cells to Con A and PHA was unaffected by GaAs, but that of B cells to LPS was increased by 52%. The delayed hypersensitivity response to keyhole limpet hemocyanin and mixed lymphocyte response were significantly reduced in a dose-dependent manner by GaAs exposure. Natural killer cell activity against the YAC-1 mouse lymphoma was enhanced in treated mice. Analysis of peritoneal exudate cells (PEC) revealed a dose-dependent decrease in number and a shift in the composition of PECs. The percentage of PEC monocytes increased from 53% of the population to 81%, while the lymphocytes decreased from 46 to 20%. The adherent PEC population demonstrated decreased phagocytosis of covaspheres and increased phagocytosis of chicken erythrocytes (CRBC). GaAs exposure had no effect on host resistance to Plasmodium yoelii or Streptococcus pneumoniae, but dose dependently increased resistance of the mouse to Listeria monocytogenes. Treated mice demonstrated a significantly decreased resistance to the B16F10 melanoma with a sevenfold increase in tumor burden at 200 mg/kg. GaAs affects both humoral and cellular immune parameters in mice and impairs the ability of the immune system to protect against B16F10 tumor challenge.
E E Sikorski, and
J A McCay, and
K L White, and
S G Bradley, and
A E Munson
January 1994,
Drug and chemical toxicology,
E E Sikorski, and
J A McCay, and
K L White, and
S G Bradley, and
A E Munson
January 1994,
Drug and chemical toxicology,
E E Sikorski, and
J A McCay, and
K L White, and
S G Bradley, and
A E Munson
August 1997,
Drug and chemical toxicology,
E E Sikorski, and
J A McCay, and
K L White, and
S G Bradley, and
A E Munson
January 1994,
Drug and chemical toxicology,
E E Sikorski, and
J A McCay, and
K L White, and
S G Bradley, and
A E Munson
January 1994,
Drug and chemical toxicology,
E E Sikorski, and
J A McCay, and
K L White, and
S G Bradley, and
A E Munson
April 1997,
Solid state nuclear magnetic resonance,
E E Sikorski, and
J A McCay, and
K L White, and
S G Bradley, and
A E Munson
August 2004,
Toxicology and applied pharmacology,
E E Sikorski, and
J A McCay, and
K L White, and
S G Bradley, and
A E Munson
May 2001,
Drug and chemical toxicology,
E E Sikorski, and
J A McCay, and
K L White, and
S G Bradley, and
A E Munson
January 1986,
Occupational medicine (Philadelphia, Pa.),
E E Sikorski, and
J A McCay, and
K L White, and
S G Bradley, and
A E Munson
September 2006,
Nano letters,
