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Maternal nicotine exposure leads to higher liver oxidative stress and steatosis in adult rat offspring
- Conceição, E.P., Peixoto-Silva, N., Pinheiro, C.R., Oliveira, E., Moura, E.G., Lisboa, P.C.
- Food and chemical toxicology 2015 v.78 pp. 52-59
- adulthood, adults, albumins, bilirubin, catalase, glutathione peroxidase, insulin, insulin resistance, lactation, liver, long term effects, nicotine, obesity, oxidative stress, progeny, protein content, rats, signal transduction, superoxide dismutase, toxicology, triacylglycerols
- Early nicotine exposure causes future obesity and insulin resistance. We evaluated the long-term effect of the maternal nicotine exposure during lactation in liver oxidative status, insulin sensitivity and morphology in adult offspring. Two days after birth, osmotic minipumps were implanted in the dams: nicotine (N), 6 mg/kg/day for 14 days or saline (C). Offspring were killed at 180 days. Protein content of superoxide dismutase, glutathione peroxidase, catalase, nitrotyrosine, 4HNE, IRS1, Akt1 and PPARs were measured. MDA, bound protein carbonyl content, SOD, GPx and catalase activities were determined in liver and plasma. Hepatic morphology and triglycerides content were evaluated. Albumin and bilirubin were determined. In plasma, N offspring had higher catalase activity, and SOD/GPx ratio, albumin and bilirubin levels but lower MDA content. In liver, they presented higher MDA and 4HNE levels, bound protein carbonyl content, SOD activity but lower GPx activity. N offspring presented an increase of lipid droplet, higher triglyceride content and a trend to lower PPARα in liver despite unchanged insulin signaling pathway. Early nicotine exposure causes oxidative stress in liver at adulthood, while protect against oxidative stress at plasma level. In addition, N offspring develop liver microsteatosis, which is related to oxidative stress but not to insulin resistance.