谷胱甘肽过氧化物酶
TBARS公司
谷胱甘肽
过氧化氢酶
内科学
硫代巴比妥酸
脂质过氧化
内分泌学
胰岛素抵抗
氧化应激
生物
化学
医学
超氧化物歧化酶
后代
抗氧化剂
胰岛素
生物化学
酶
怀孕
遗传学
作者
Thaís Verônica Saori Tsosura,Rodrigo Martins dos Santos,Antonio Hernandes Chaves‐Neto,Fernando Yamamoto Chiba,Ana Carolina Nascimento Carnevali,Maria Sara de Lima Coutinho Mattera,Bianca Elvira Belardi,Luciano Tavares Ângelo Cintra,Nathália Evelyn da Silva Machado,Dóris Hissako Sumida
标识
DOI:10.1016/j.joen.2021.04.003
摘要
Abstract
Introduction
Maternal apical periodontitis (AP) is associated with insulin resistance (IR) in adult offspring. Oxidative stress has been linked to IR. This study investigated insulin sensitivity (IS) and oxidative stress in the gastrocnemius muscle (GM) of adult offspring of rats with AP. Methods
Fifteen female Wistar rats were distributed into a control group, a group with 1 tooth with AP, and a group with 4 teeth with AP. Thirty days after AP induction, female rats were mated with healthy male rats. When male offspring reached 75 days of age, glycemia, insulinemia, and IS were determined. In the GM, the oxidative damage products (thiobarbituric acid reactive substances and carbonyl protein) and activities of enzymatic (superoxide dismutase, catalase, and glutathione peroxidase) and nonenzymatic (glutathione and total antioxidant capacity) antioxidants were quantified. Analysis of variance was performed followed by the Tukey post hoc test (P < .05). Results
Maternal AP was associated with decreased IS and changes in antioxidant activities (reduced superoxide dismutase and increased catalase, glutathione peroxidase, and glutathione) and decreased thiobarbituric acid reactive substance concentration in the GM of their adult offspring. However, maternal AP does not appear to affect glycemia, carbonyl protein concentration, and the nonenzymatic total antioxidant capacity in the GM of this offspring. Conclusions
Maternal AP modulates the antioxidant defense system in the GM of their adult offspring, attenuating lipid peroxidation in this tissue. This reflects part of an adaptive response of the offspring to the stimulation of the maternal chronic oral inflammatory process in which the organism acts by decreasing oxidative tissue damage in the postnatal stage. The present study improves knowledge about the impact of maternal oral inflammation on healthy offspring.
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