Toxicological Sciences, Vol 50, 244-248, Copyright © 1999 by Society of Toxicology
G Garcia-Arenas, L Claudio, F Perez-Severiano and C Rios
The toxicity of lead (Pb) is of concern to public health due to its
persistence in the environment. Brain is one of the major target organs
where severe neurologic alterations may be triggered after exposure. The
primary effects of lead on brain functions are thought to be a damage to
the nervous system microvasculature. However, the mechanism of this
toxicity is poorly understood. Nitric oxide synthase (NOS) may be a target
for lead and changes in its function can result in a cascade of
pathophysiological effects that may be observed in isolated capillaries and
synaptosomes. We have determined the concentration of lead in blood,
capillaries and synaptosomes in brain from mice receiving 0, 250, 500, and
1000 ppm of lead for 14 days, through the drinking water. NOS activity was
determined in the capillaries and synaptosomes by following the conversion
of 3H-L-arginine to 3H-L- citrulline. The results show that blood lead
levels were dose- dependent. Brain capillaries showed a preferential
accumulation of lead as compared to synaptosomes. With all Pb treatments,
synaptosomal constitutive NOS was inhibited (about 50% of control) while
the inducible NOS activity in capillaries was enhanced. These data suggest
that inhibition of cNOS activity and increase in iNOS may contribute to the
Pb effects on the CNS.
ARTICLES
Lead acetate exposure inhibits nitric oxide synthase activity in capillary and synaptosomal fractions of mouse brain
Area de Toxicologia, Centro Nacional de Salud Ambiental, SSA, Mexico.
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