J. Bernier et al., IMMUNOTOXICITY OF AMINOCARB .3. EXPOSURE ROUTE-DEPENDENT IMMUNOMODULATION BY AMINOCARB IN MICE, Toxicology, 99(1-2), 1995, pp. 135-146
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.