IMMUNOTOXICITY OF AMINOCARB .3. EXPOSURE ROUTE-DEPENDENT IMMUNOMODULATION BY AMINOCARB IN MICE

Aminocarb, a phenylsubstituted methylcarbamate pesticide (4-dimethylam ino-3-methyl-N-carbamate; matacil), previously suspected of a relative ly low immunotoxic potential, was administered by four different expos ure routes to C57BL/6 mice. A single sublethal exposure by oral and de rmal routes stimulated humoral immune response at a relatively low dos e; 1/256 LD(50) of aminocarb. Intraperitoneal (i.p.) injection decreas ed the humoral PFC response, whereas inhalation of aminocarb had no ma rked effect on peripheral immune status in exposed animals. Thus, i.p. exposure resulted in higher immunotoxicity over oral administration o f aminocarb. Similarly, marked route-related exposure differences in i mmunomodulatory effects of aminocarb were noted for mitogenic stimulat ion of spleen lymphocytes and mixed lymphocyte response. Other indices , such as delayed type hypersensitivity (DTH) and production of interl eukin-2 (IL-2) were unchanged. Interestingly, expression of major hist ocompatibility complex (MHC) class II by purified, lipopolysaccharide (LPS)-stimulated B cells increased equally after i,p. and oral exposur es to aminocarb. Overall, a weak immunosuppressive potential of aminoc arb was concluded, which was possibly due to indirect interaction of t he pesticide with the immune system. However, aminocarb may represent an autoimmunity-inducing toxic.