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Published on: January 27, 2019
Developmental toxicity of cesium in the mouse
1Texas Tech University Health Sciences Center, School of Medicine, Lubbock 79430.
Abstract:
1. Maternal intake of 1 mEq CsCl in drinking water at conception until weaning the offspring mice resulted in certain maternal mediated neonatal and developmental toxicity. 2. Initial reduction in body and brain weights were determined in male offspring due to maternal exposure to Cs salt before they attained the control levels. 3. Offspring from both sexes showed increased spleen weight from control as a consequence of maternal exposure to Cs. This may precipitate delayed immunotoxicity. 4. Maternal Cs exposure did not alter litter size or specific activities of offspring heart lactate dehydrogenase isoenzymes from respective controls. 5. Maternal exposure to Cs altered specific activities of offspring liver alcohol- and aldehyde dehydrogenase during development compared to controls. 6. The results indicate neonatal and developmental toxicity of Cs as a function of maternal intake of CsCl during pregnancy and breast feeding.
Insights
Maternal cesium chloride (CsCl) intake during pregnancy and nursing caused neonatal and developmental toxicity in mice offspring. Exposure led to reduced body/brain weights in males and increased spleen weights in both sexes, indicating potential immunotoxicity.
Area of Science:
- Toxicology
- Developmental Biology
- Environmental Health
Background:
- Cesium chloride (CsCl) is a chemical compound with potential health implications.
- Understanding the effects of maternal exposure to CsCl on offspring development is crucial for public health.
- Neonatal and developmental toxicity studies are essential for risk assessment.
Purpose of the Study:
- To investigate the neonatal and developmental toxicity of maternal cesium chloride (CsCl) intake.
- To assess the impact of CsCl exposure on offspring growth, organ weights, and enzyme activities.
- To determine the consequences of maternal CsCl ingestion during gestation and lactation.
Main Methods:
- Pregnant mice received 1 mEq CsCl in drinking water from conception until offspring weaning.
- Offspring body and brain weights were measured.
- Spleen weights were assessed in offspring.
- Lactate dehydrogenase (LDH) isoenzyme activities in heart and liver alcohol/aldehyde dehydrogenase activities were analyzed.
Main Results:
- Maternal CsCl intake resulted in neonatal and developmental toxicity.
- Male offspring exhibited reduced body and brain weights.
- Both male and female offspring showed increased spleen weights, suggesting potential immunotoxicity.
- Specific activities of liver alcohol and aldehyde dehydrogenase were altered in offspring.
Conclusions:
- Maternal CsCl intake during pregnancy and lactation induces significant neonatal and developmental toxicity in mice.
- Observed effects include growth retardation and potential immunotoxicity, highlighting the risks of cesium exposure.
- Cesium chloride exposure during critical developmental periods warrants further investigation and precautionary measures.
