Jan 1, 1977

Tri-O-tolyl phosphate neurotoxicity: lack of evidence for autoimmunologic involvement

Archives of Environmental Contamination and Toxicology
P G Watanabe, R P Sharma


Studies on the involvement of autoimmunity in the pathogenesis of tri-O-tolyl phosphate (TOTP) induced neurotoxicity in chickens were conducted. Immunosuppressive therapy including gamma-radiation and drug treatments was utilized to determine its effects on the neurotoxic syndrome. Whole-body gamma-irradiation up to 1020 roentgens failed to show any consistent protection from the TOTP induced paralysis. Therapy involving prednisone alone or in combination with 6-mercaptopurine and antilymphocyte serum likewise indicated no protection. Stimulation of humoral and cellular immunity by TOTP was investigated. Complement fixation, precipitation tests, splenic migration inhibition, and skin tests did not indicate stimulation of autoimmunity toward nervous tissue or liver. The present investigation was unable to demonstrate primary involvement of an autoimmune nature in the neurotoxicity produced by TOTP in the chicken.

Mentioned in this Paper

Poliomyelitis, Bulbar
Pathogenic Aspects
Precipitin Tests
Phosphate Measurement
Neoplasms, Nerve Tissue
Tritolyl Phosphates
Autoimmune Diseases

About this Paper

Related Feeds

Autoimmune Hepatitis

Autoimmune hepatitis formerly called lupoid hepatitis, is a chronic, autoimmune disease of the liver that occurs when the body's immune system attacks liver cells causing the liver to be inflamed. Discover the latest research on autoimmune hepatitis here.

Autoimmune Diseases

Autoimmune diseases occur as a result of an attack by the immune system on the body’s own tissues resulting in damage and dysfunction. There are different types of autoimmune diseases, in which there is a complex and unknown interaction between genetics and the environment. Discover the latest research on autoimmune diseases here.

Antibodies: Complement Activation

The complement system can be activated by antigen-associated antibody. In the classical pathway of complement activation, C1q, C4b, and C3b are all able to bind to the Fc portion of IgG or IgM. Find the latest research on antibodies and complement activation here.