TY  - JOUR
PY  - 1998//
TI  - Poisons and fever
JO  - Clinical and experimental pharmacology and physiology
A1  - Gordon, C. J.
A1  - Rowsey, P. J.
SP  - 145
EP  - 149
VL  - 25
IS  - 2
N2  - 1. Dysfunction of the thermoregulatory system is one of many pathologies documented in experimental animals and humans exposed to toxic chemicals. The mechanism of action responsible for many types of poison-induced fevers is not understood. Some elevations in body temperature are attributed to the peripheral actions of some poisons that stimulate metabolic rate and cause a forced hyperthermia. Exposure to organophosphate (OP) pesticides and certain metal fumes appears to cause a prolonged, regulated elevation in body temperature (Tb). 2. Activation of cyclo-oxygenase (COX) and the production of prostaglandin (PG)E2 in central nervous system (CNS) thermoregulatory centres is required to elicit a fever. Activating the COX-PGE2 pathway by a poison may occur by one of three mechanisms: (i) induction of cell-mediated immune responses and the subsequent release of cytokines; (ii) induction of lipid peroxidation in the CNS; and (iii) direct neurochemical activation. 3. Radiotelemetric monitoring of core temperature in unstressed rodents has led to an experimental animal model of poison-induced fever. Rats administered the OP agents chlorpyrifos and diisopropyl fluorophosphate display an initial hypothermic response lasting approximately 24 h, followed by an elevation in diurnal core temperature for 24-72 h after exposure. The hyperthermia is apparently a result of the activation of the COX-PGE2 pathway because it is blocked by the anti-pyretic sodium salicylate. Overall, the delayed hyperthermia resulting from OP exposure involves activation of thermoregulatory pathways that may be similar to infection-mediated fever.<p /> <p>Language: en</p>
LA  - en
SN  - 0305-1870
UR  - http://dx.doi.org/
ID  - ref1
ER  -