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Alterations of motor nerve functions in animals exposed to motorcycle exhaust
Shing-Hwa Liu1, Jei-Hui Wang, Jiunn-Jye Chuu
1Institute of Toxicology, Medical College, National Taiwan University, Taipei, Taiwan. shliu@ha.mc.ntu.edu.tw
Abstract:
The effect of motorcycle exhaust (ME) on the motor nerve was studied using animals exposed to the exhaust by inhalation, intratracheal, or intraperitoneal administration of ME particulate (MEP). A 4-wk ME inhalation and intratracheal instillation of MEP for 1 d in rats or intraperitoneal administration of MEP (0.5 g/kg/d for 1 d and 0.1 g/kg/d for 2 d) in mice significantly decreased both rota-rod performance and motor nerve conduction velocity. The effect of some polycyclic aromatic hydrocarbons on the motor nerve was also investigated. Treatment with benzo[a]pyrene (0.05 and 0.1 g/kg/d for 3 d), but not pyrene (0.1 g/kg/d for 3 d), resulted in significant decrease of motor nerve conduction velocity in mice. Moreover, the Na(+),K(+)-ATPase activities of sciatic nerves isolated from ME-, MEP-, or benzo[a]pyrene-exposed animals were decreased. Treatment with pyrene did not markedly affect the Na(+),K(+)-ATPase activity of sciatic nerve. The rats exposed to ME for 4 wk showed increases in blood and sciatic nerve manganese levels. Results indicate that motorcycle exhaust produces adverse effects on the motor nerve, which is associated with a fall in nerve Na(+),K(+)-ATPase activity.
Insights
Motorcycle exhaust (ME) exposure negatively impacts motor nerve function in animal models. This neurotoxicity is linked to reduced nerve conduction velocity and impaired Na(+),K(+)-ATPase activity, suggesting potential health risks.
Area of Science:
- Environmental toxicology
- Neuroscience
- Occupational health
Background:
- Motorcycle exhaust (ME) is a complex mixture of pollutants.
- Potential neurotoxic effects of ME exposure require thorough investigation.
- Polycyclic aromatic hydrocarbons (PAHs) are known components of ME with potential health impacts.
Purpose of the Study:
- To investigate the neurotoxic effects of motorcycle exhaust (ME) on motor nerve function.
- To determine the role of ME particulate (MEP) and specific PAHs in motor nerve damage.
- To elucidate the underlying mechanisms of ME-induced neurotoxicity.
Main Methods:
- Animal models (rats and mice) were exposed to ME via inhalation, intratracheal instillation of MEP, or intraperitoneal administration.
- Motor nerve function was assessed using rota-rod performance and motor nerve conduction velocity tests.
- Na(+),K(+)-ATPase activity in sciatic nerves was measured.
- Blood and sciatic nerve manganese levels were analyzed in ME-exposed rats.
Main Results:
- ME inhalation and MEP administration significantly reduced motor nerve conduction velocity and rota-rod performance in rodents.
- Benzo[a]pyrene exposure decreased motor nerve conduction velocity, while pyrene did not.
- Na(+),K(+)-ATPase activity in sciatic nerves was significantly reduced following exposure to ME, MEP, or benzo[a]pyrene.
- ME exposure in rats led to increased blood and sciatic nerve manganese levels.
Conclusions:
- Motorcycle exhaust exerts adverse effects on motor nerve function.
- Reduced Na(+),K(+)-ATPase activity is a key mechanism underlying ME-induced neurotoxicity.
- Specific components like benzo[a]pyrene contribute to ME's neurotoxic potential.
- Manganese accumulation may play a role in ME neurotoxicity.