ACUTE AND SUBCHRONIC IMMUNOTOXICITY OF P-CHLORONITROBENZENE IN MICE -I - EFFECT ON NATURAL-KILLER, CYTOTOXIC T-LYMPHOCYTE ACTIVITIES AND MITOGEN-STIMULATED LYMPHOCYTE-PROLIFERATION
Citation
Q. Li et al., ACUTE AND SUBCHRONIC IMMUNOTOXICITY OF P-CHLORONITROBENZENE IN MICE -I - EFFECT ON NATURAL-KILLER, CYTOTOXIC T-LYMPHOCYTE ACTIVITIES AND MITOGEN-STIMULATED LYMPHOCYTE-PROLIFERATION, Toxicology, 127(1-3), 1998, pp. 223-232
Categorie Soggetti
Toxicology,"Pharmacology & Pharmacy
SICI code
0300-483X(1998)127:1-3<223:AASIOP>2.0.ZU;2-A
Abstract
We evaluated the immunotoxicity of p-chloronitrobenzene (p-CNB) after
intraperitoneal (ip) injection of p-CNB in BDF1 mice; single ip inject
ion of 300 mg/kg (acute experiments), or 30 mg/kg three times a week f
or 4 weeks (subchronic experiments).The following items were investiga
ted: number of splenocytes, natural killer (NK) activity, cytotoxic T-
lymphocyte (CTL) activity and LPS-stimulated lymphocyte proliferation
using splenocytes, hemoglobin (Hb) concentration in peripheral blood a
nd body weight. NK activity in exposed mice significantly decreased co
mpared to control in both acute and subchronic experiments. CTL activi
ty in acute exposed mice showed a significant decrease on the 3rd day
only after injection, and significant decrease at 3 and 4 weeks in sub
chronic exposed mice compared to controls. Comparing the effect of p-C
NB on NK activity with that of CTL for both the acute and subchronic e
xposures, NK activity was more inhibited by p-CNB than CTL activity in
the acute stage, whereas both the NK and CTL activities were inhibite
d by p-CNB in the subchronic stage. There was an indication that p-CNB
also inhibited LPS- stimulated B-lymphocyte proliferation. On the oth
er hand, Hb concentration did not show significant difference between
the exposed and control mice in both acute and subchronic experiments.
Body weight in subchronically exposed mice was significantly lower th
an the control from day 19. The above evidence indicated that p-CNB ha
s an inherent immunotoxic effect on mice. (C) 1998 Elsevier Science Ir
eland Ltd. All rights reserved.