Organophosphates are some the widely used pesticides in the world, their mechanism of acute toxicity is associated with inhibiting acetylcholinesterase (AChE). Recently, increasing attention has been put to paraoxonase (PON1) which hydrolyzes OPs and prevents atherosclerosis by its anti-oxidation effects on low density lipoproteins (LDLs), resulted in decreased pro-inflammatory lipid peroxides formation. Since vascular endothelial dysfunction is known as the primary step in atherogenesis, the influence of OPs on the vascular endothelial function was assessed. Results showed that trichlorfon (18 mg·kg^-1) intragastrically daily for 70 days in rabbits resulted in a significant inhibition of endothelium-dependent relaxation (EDR), a decrease of endothelium nitric oxide synthase (eNOS) activity in isolated aorta and the changes of biochemical parameters in plasma, including a decrease of superoxide dismutase (SOD), PON1 and AChE activity and nitric oxide level and an increase of malondialdehyde (MDA) level. In addition, a direct exposure of rabbit aortic rings to paraoxon also inhibited EDR. These findings suggest that subchronic toxicity dose intragastrically trichlorfon or vessels to be exposed directly to paraoxon in vitro could induce dysfunction of vascular endothelium. The mechanisms may involve an inhibition of antioxidases and oxidative stress induced by OPs.