Disease relevance of Surecide

• Protective effect of pretreatment against the acute toxicity of formulated cyanofenphos in hens [1].
• However, about 10 to 15 days later leptophos- and cyanofenphos-treated chickens developed the characteristic leg weakness and unrecoverable ataxia seen in birds given TOCP [2].

High impact information on Surecide

• In vivo inhibition of chicken brain acetylcholinesterase and neurotoxic esterase in relation to the delayed neurotoxicity of leptophos and cyanofenphos [2].
• Biochemically, it was found that duck brain neurotoxic esterase (NTE) activity was inhibited in vivo to less than 15% of control levels as measured 24 h after the last treatment with TOCP, leptophos, or cyanofenphos [3].
• The oral LD50 for formulated cyanofenphos was 700 mg/kg in the control hens and 1170 mg/kg in the hens pretreated with 10 mg/kg daily for 8 days [1].
• Histopathologic examinations indicated that degenerative lesions of axons consistent with the type occurring in delayed neurotoxicity were seen in all TOCP-, leptophos-, or cyanofenphos-treated ducks and were specially evident in sections of spinal cord [3].
• Five organophosphorous insecticides: Leptophos, EPN, Cyanofenphos, trichloronate and salithion proved to cause irreversible ataxia not only to chicken but also to mice and sheep [4].

Gene context of Surecide

• The protective effect of pretreatment against the acute toxicity of formulated cyanofenphos appears to be related to the fact that the formulation produced less inhibition of brain AChE activity in the pretreated hens than in the controls [1].

References