Efeitos da restrição proteica perinatal na segunda geração de ratas jovens: avaliação do metabolismo oxidativo hepático da prole

The restriction of maternal nutrients during the critical period of development is being singled out as one of the main factors in the onset of chronic diseases in adulthood. Thus, the objective was to study the function and hepatic oxidative metabolism of the second generation of young rats subjected to perinatal protein restriction, and its correlation with metabolic diseases in adulthood. Rats were used Wistar. The study was approved by the Ethics Committee on Animal studies with the Biological Sciences Center of UFPE (N° 23076.018417/2013-73). The pregnant rats were divided into two groups according to the diet provided: control (C, 17% casein) and malnourished (D, casein, 8%). In lactation, the rats continue to receive experimental diet as the experimental group and after weaning (21 days old) pups received vivarium diet Presence-Purina®. Animals born from the first mating (F1) after growth, were mated to obtain the second generation (F2). Males (F2) were evaluated at 30 days old. We evaluated the body weight and hepatic tissue, and the relative weight of the liver to body weight, lipid peroxidation (MDA) levels, protein oxidation (carbonyl) sulfhydryl groups (SH), reduced glutathione (GSH), and the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and Glucose- 6-phosphate dehydrogenase (G6PDH). There was a decrease in body weight (C=3,54 ± 101 n=8 vs D=87,6 ± 2,46g n=8 p<0.01) and in liver weight (C= 4,10 ± 0.15, n=6 vs D=3,48 ± 0.18g n=6 p<0.05), and increased relative weight in malnourished animals in the control group (C=3,742 ± 0,1402 n=5; D=4,452 ± 0,2137g n=5 p<0.05). MDA levels (C= 19.11 ± 0.94, n=10 vs D=12,10 ± 1,07 nmol/mg protein (Prot.) n=8 p<0.001) and carbonyl (C=7.242 ± 0.45, n=5 vs D=4.495 ± 0.43 nmols/mg prot., n=6, p<0.01) were lower in the unfed group, since the levels of sulfhydryl groups (C=0.06 ± 0.004, n=4 vs D=0.076 ± 0.002 nmol/mg prot., n=5, p<0.01) and GSH (C=36.76 ± 1.83, n=6, vs 46.96 ± D=1, 56 μmol/mg prot., n=6, p<0.01) increased in the malnourished animals compared to the control group. In relation to the antioxidant enzymes SOD activity (C=184.6 ±15.90, n= 8 vs D=363.8 ± 89.87 U/mg prot. n=8 p=0.06) and CAT (C= 13.7 ± 0.78, n=8 vs D= 15.98 ± 0.61 U/mg prot. n=9 p<0.05) increased in malnourished animals, but these animals was reduced GPx (C=5,27 ± 0,26 n=7 vs D=4,16 ± 0,13 U/mg prot. n=7 p<0.01) and the activity of GST (C=18,19 ± 230,8 n=5 vs D=375,3 ± 7,25 U/mg prot., n=6, p<0.0001) and G6PDH (C=63,65 ± 14,26 n=5 vs D=127,8 ± 7,70 nmol/min/mg prot., n=5, p<0.01) was increased in malnourished animals compared to the control group. Our results suggest that the livers of the F2 animals are more resistant to the effects of perinatal protein restriction, since it did not have an oxidative stress frame, before that, we can assume that these animals are an attempt to maintain metabolic homeostasis on the nutritional insult suffered the critical period of development in the previous generation (F1).