Abstract
We evaluated the immunotoxicity of p-chloronitrobenzene ( p-CNB) after intraperitoneal (ip) injection of p-CNB in BDF1 mice; single ip injection of 300 mg/kg (acute experiments), or 30 mg/kg three times a week for 4 weeks (subchronic experiments). The following items were investigated: 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 and body weight. NK activity in exposed mice significantly decreased compared to control in both acute and subchronic experiments. CTL activity in acute exposed mice showed a significant decrease on the 3rd day only after injection, and significant decrease at 3 and 4 weeks in subchronic exposed mice compared to controls. Comparing the effect of p-CNB on NK activity with that of CTL for both the acute and subchronic exposures, NK activity was more inhibited by p-CNB than CTL activity in the acute stage, whereas both the NK and CTL activities were inhibited by p-CNB in the subchronic stage. There was an indication that p-CNB also inhibited LPS- stimulated B-lymphocyte proliferation. On the other 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 than the control from day 19. The above evidence indicated that p-CNB has an inherent immunotoxic effect on mice.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.