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Modulation of DNA damage by vitamin A in developing Sprague-Dawley rats
C Bolognesi1, E Ognio, L Ferreri-Santi
1Istituto Nazionale per la Ricerca sul Cancro-IST, Università di Genova, Italy.
Abstract:
Prenatal and neonatal Sprague-Dawley rats were given a diet deficient in or with an excess of Vitamin A and at the age of 55 days female progeny were treated with a single i.g. dose of 80 mg/kg DMBA or 50 mg/kg MNU. Under these experimental conditions it was found that the exposure of perinatal rats to a diet containing an excess of Vitamin A caused a decrease in the amount of DMBA- and MNU-induced DNA damage in the mammary gland and the liver of the female offspring. When diets were deficient in Vitamin A there was a dual effect in terms of DNA damage detected in the same organs, namely DMBA caused an amount of DNA damage comparable to controls, while the extent of DNA damage induced by MNU greatly increased in both organs. These results indicate that Vitamin A can permanently change the sensitivity of adult progeny to chemically induced DNA damage when it is given to pregnant and lactating females.
Insights
Maternal Vitamin A intake influences offspring
Area of Science:
- Nutritional Science
- Toxicology
- Developmental Biology
Background:
- Vitamin A is crucial for development.
- Maternal nutrition impacts offspring health.
- Chemical carcinogens can induce DNA damage.
Purpose of the Study:
- To investigate the effects of maternal Vitamin A levels on offspring's susceptibility to DNA damage.
- To assess the impact of prenatal and neonatal Vitamin A exposure on chemically induced DNA damage.
Main Methods:
- Sprague-Dawley rats received diets deficient in or in excess of Vitamin A during prenatal and neonatal periods.
- Female offspring were treated with dimethylbenz[a]anthracene (DMBA) or N-methyl-N-nitrosourea (MNU) at 55 days old.
- DNA damage in mammary gland and liver tissues was quantified.
Main Results:
- Excess Vitamin A reduced DMBA- and MNU-induced DNA damage.
- Vitamin A deficiency led to increased MNU-induced DNA damage but comparable DMBA-induced damage.
- Organ-specific differences in DNA damage response were observed.
Conclusions:
- Maternal Vitamin A status can permanently alter offspring's susceptibility to chemical carcinogens.
- Vitamin A plays a significant role in modulating DNA repair mechanisms or cellular defense against genotoxicity.
- These findings highlight the importance of maternal nutrition in long-term offspring health and cancer risk.