Undernutrition in the parental and first generation provokes an organ‐specific response to oxidative stress on neonates of second filial generation of Wistar rats

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Undernutrition results from the deficit of some or all the macro‐ and micronutrients caused primarily by lack of food. During pregnancy, this condition modifies the structure and function of the placenta such as glucose, amino acids and fatty acids transportation (Belkacemi et al., 2010; Ayuk et al., 2012). A reduction in the food intake during pregnancy increases levels of cholesterol, triglycerides and adiponectin in the offspring (Lukasewski et al., 2011; Lee et al., 2013) and modifies the expression of proteins related to obesity and foetal programming (Lee et al., 2015), which can alter the normal proliferation, differentiation and maturation of the cell producing adaptations that permanently changes the physiology and metabolism of several tissues and organs that lead to ensure of survival of offspring (Godfrey and Barker, 2001; Drake and Walker, 2004; Belkacemi et al., 2010; Entringer et al., 2012), although with a higher risk for development of diseases in adulthood such as small‐bowel mucosal atrophy which decrease digestion capacity and absorption of nutrients (Müller and Krawinkel, 2005). Risk is increased in male offspring, because during the pregnancy the food restriction produces a modification in proteins expression related with one‐carbon metabolism in these but not in females (You et al., 2015).
During undernutrition also occurs a decrease in endogenous antioxidant levels that cause a rapid increase of intracellular levels of reactive oxygen species (ROS) (Fechner et al., 2001), producing a chronic oxidative stress which alters the structure and function of different macromolecules (Squali Houssaïni et al., 2001; Wen et al., 2002; Salmon et al., 2004), increasing the apoptosis (Robertson, 2004). Oxidative stress produced by foetal undernutrition affects germinal cells producing a premature ageing in the ovaries (Bernal et al., 2010). Moreover, the oxidant molecules can modify the DNA methylation patterns, producing epigenetic changes (Thompson and Al‐Hasan, 2012), whereupon several generations are affected through epigenetic inheritance and transgenerational reprogramming (Wu et al., 2004; Drake et al., 2005; Dunn et al., 2011). Recent studies suggest that epigenetic modifications produced in sperm of the offspring may be transmitted to somatic cell of next generations altering the metabolic response and increasing the risk factors of that F1 and F2 generations to develop non‐communicable diseases (Martinez et al., 2014; Radford et al., 2014).
On the other hand, Pickering et al. (2013) demonstrated that repeated exposure to low oxidant levels by short times results in an adaptation to oxidative stress. So it is likely that a chronic state of intergenerational oxidative stress caused by undernutrition can lead to the foetus to develop a biochemical adaptation that reduces oxidative damage to ensure the survival of organism. The aim of this study was to determine the effect of intergenerational undernutrition on protein oxidation and the antioxidant defence response on liver, heart and brain in the second filial generation (F2) of undernourished neonate rats, descendants of parents (both parental and first generation) fed a low‐nutrient diet. This study may provide an insight on how organs of neonates of the second filial generation respond to oxidative stress caused by intergenerational undernutrition.
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