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Lead acetate delays rapid postnatal mouse brain and body growth
H T Epstein1, K Fenton, S Shimpach
1Biology Department, Brandeis University, Waltham, MA 02254.
Insights
Maternal lead exposure in mice significantly slows offspring body and brain growth, delaying key developmental stages. This early developmental impact highlights lead
Area of Science:
- Developmental Toxicology
- Neuroscience
- Environmental Health
Background:
- Lead (Pb) is a known developmental toxicant.
- Prenatal and early postnatal exposure can impact growth and neurodevelopment.
Purpose of the Study:
- To investigate the effects of maternal lead acetate exposure on mouse offspring growth and brain development.
- To determine the timing and severity of developmental delays caused by lead exposure.
Main Methods:
- Mothers of mouse litters received either tap water or lead acetate (10 mg/ml) in drinking water from parturition to weaning.
- Offspring body weight, brain weight, and developmental milestones were monitored.
Main Results:
- Lead-exposed offspring exhibited significantly lower body weights and a 2-day delay in the onset of rapid body growth.
- Significantly smaller brain weights were observed in lead-exposed offspring between 14 days and weaning.
- The onset of rapid brain growth was delayed by approximately 4-6 days in lead-exposed mice.
Conclusions:
- Maternal lead exposure during early development causes significant delays in both body and brain growth in mice.
- The initial impact on brain growth is more pronounced than on body growth, though brain weight recovers partially by 26 days.
- These findings underscore the critical vulnerability of early development to lead toxicity.
Abstract:
Starting at parturition and continuing until weaning, mothers of five mouse litters received tap water while five others had 10 mg PbAc/ml in their drinking water. The offspring receiving lead from the mothers had significantly lower body weights after the first days of receiving lead; their slowed body growth led to a 2-day delay of onset (usually at 16-18 days) of their last rapid body growth stage. They also had significantly smaller brain weights between age 14 days and weaning (23 days). The onset of rapid brain growth was delayed from its usual onset at 16-18 days to about 22-23 days before rising to about the same value as the control mice at 26 days. Thus, the initial effect on brain growth is decidedly greater than on body growth, though brain weight later reaches close to the control value.