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Neonatal lead toxicity and in vitro lipid peroxidation of rat brain
Insights
Lead exposure in neonatal rats did not accelerate brain lipid peroxidation. Despite effects on growth and hematocrit, lead toxicity did not increase malondialdehyde formation in brain tissue.
Area of Science:
- Neuroscience
- Toxicology
- Developmental Biology
Background:
- Neonatal lead (Pb) exposure can cause central nervous system (CNS) toxicity.
- Lipid peroxidation is a potential mechanism contributing to Pb-induced neurotoxicity.
Purpose of the Study:
- To investigate the relationship between neonatal lead exposure and in vitro lipid peroxidation in rat brain tissue.
- To determine if lead exposure alters malondialdehyde (MDA) formation in neonatal rat brains.
Main Methods:
- Neonatal rats were administered aqueous lead acetate intragastrically from day 2 to 20 at varying doses.
- Blood lead concentrations, growth, and hematocrits were measured.
- Malondialdehyde (MDA) formation in brain supernatants was assessed spontaneously and induced by superoxide anion.
- In vitro addition of lead to brain supernatants was performed to assess direct effects on MDA formation.
Main Results:
- Significant growth depression and decreased hematocrits were observed at the highest lead dose.
- Spontaneous and superoxide-induced MDA formation in brain supernatants were not significantly altered by lead exposure in vivo.
- In vitro, lead significantly decreased MDA formation at concentrations of 10(-5) M and higher.
Conclusions:
- Neonatal lead exposure in rats does not lead to accelerated in vitro lipid peroxidation of brain tissue.
- The observed CNS toxicity of lead in neonates is not mediated by increased lipid peroxidation in the brain.
- Lead may directly inhibit lipid peroxidation in brain tissue in vitro.
Abstract:
Neonatal rats were given aqueous lead acetate intragastrically from d 2--20 of life at doses of 0, 25, 75, and 225 mg Pb/kg.d. Blood Pb concentrations on d 21 were (mean +/- SE) 27 +/- 4 (control), 150 +/- 26, 263 +/- 63, and 518 +/- 97 microgram/100 ml, respectively. Growth was significantly depressed only in animals given the highest dose of Pb (225 mg/kg.d). Hematocrits were significantly decreased by d21 at all doses of Pb. Malondialdehyde (MDA) formation in 750 x g (10 min) brain supernatants induced spontaneously by aerobic incubation at 37 degrees C was not altered by Pb on d 7 and 14, but a slight decrease was observed on d 21. The extent of MDA formation induced by enzymatically generated superoxide anion was not altered by Pb toxicity during the first 21 d of life. Addition of Pb to 750 x g (10 min) brain supernatants in vitro significantly decreased MDA formation at Pb concentrations of 10(-5) M and higher. These results show that the central nervous system toxicity of Pb in neonatal rats is not associated with accelerated in vitro lipid peroxidation of brain tissue.