Tissue & cell · 2025
Effect of perinatal nicotine exposure on oxidative stress and BDNF levels in the brain tissue of offspring rats: The protective role of Vitamin E.
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Özerol Beyza Güzide, Selçuk Engin Burak, Gürel Elif, Üremiş Muhammed Mehdi, Gül Mehmet, Gül Semir, Bağ Harika Gözde Gözükara, Özhan Onural, Türköz Yusuf
Аннотация
OBJECTIVE: Nicotine, a well-known neurotoxin, induces oxidative stress in fetal tissues, leading to organ damage and fetal growth retardation. This study aims to evaluate oxidative stress parameters in the brain tissue of rat offspring exposed to perinatal nicotine and assess vitamin E's protective effects.
METHODS: Twenty-five pregnant rats were administered 10 mg/L of nicotine and 300 mg/L of Vitamin E in drinking water starting from the first day of gestation. On gestational day 21, some offspring were euthanized to form the prenatal group. The remaining litters were born naturally, and dams received treatments via drinking water during gestation and lactation (6 weeks). After the lactation period, the pups were weaned and directly treated for an additional 9 weeks, resulting in an overall treatment duration of 15 weeks. Brain tissues were analyzed for MDA, GSH, TOS, TAS, OSI, BDNF, Caspase-3 activity, and histopathological changes.
RESULTS: The nicotine-exposed pups exhibited significantly reduced crown-rump length, body mass, and brain mass compared to controls. Nicotine exposure decreased BDNF, GSH, and TAS levels and increased MDA, TOS, and OSI levels. Histopathologically, the nicotine prenatal group showed a significantly higher number of heterochromatic nuclei in brain tissue. Caspase-3 activity did not show a significant increase in nicotine groups compared to the control. Vitamin E supplementation mitigated nicotine-induced brain damage in some measured parameters.
CONCLUSION: Perinatal nicotine exposure induces oxidative damage in the brain tissue of rat offspring, while vitamin E exerts a protective antioxidant effect, preventing nicotine-induced neurotoxicity. Furthermore, the significant reduction in BDNF levels and the increase in heterochromatic nuclei in the nicotine-exposed groups highlight the detrimental impact of nicotine on neurodevelopment, which can be effectively mitigated by vitamin E supplementation.
METHODS: Twenty-five pregnant rats were administered 10 mg/L of nicotine and 300 mg/L of Vitamin E in drinking water starting from the first day of gestation. On gestational day 21, some offspring were euthanized to form the prenatal group. The remaining litters were born naturally, and dams received treatments via drinking water during gestation and lactation (6 weeks). After the lactation period, the pups were weaned and directly treated for an additional 9 weeks, resulting in an overall treatment duration of 15 weeks. Brain tissues were analyzed for MDA, GSH, TOS, TAS, OSI, BDNF, Caspase-3 activity, and histopathological changes.
RESULTS: The nicotine-exposed pups exhibited significantly reduced crown-rump length, body mass, and brain mass compared to controls. Nicotine exposure decreased BDNF, GSH, and TAS levels and increased MDA, TOS, and OSI levels. Histopathologically, the nicotine prenatal group showed a significantly higher number of heterochromatic nuclei in brain tissue. Caspase-3 activity did not show a significant increase in nicotine groups compared to the control. Vitamin E supplementation mitigated nicotine-induced brain damage in some measured parameters.
CONCLUSION: Perinatal nicotine exposure induces oxidative damage in the brain tissue of rat offspring, while vitamin E exerts a protective antioxidant effect, preventing nicotine-induced neurotoxicity. Furthermore, the significant reduction in BDNF levels and the increase in heterochromatic nuclei in the nicotine-exposed groups highlight the detrimental impact of nicotine on neurodevelopment, which can be effectively mitigated by vitamin E supplementation.