Many studies have shown that a maternal low-protein diet increases the susceptibility of offspring to cardiovascular disease in later-life. Moreover, a lower incidence of cardiovascular disease in females than in males is understood to be largely due to the protective effect of high levels of estrogens throughout a woman's reproductive life. However, to our knowledge, the role of estradiol in moderating the later-life susceptibility of offspring of nutrient-deprived mothers to cardiovascular disease is not fully understood. The present study is aimed at investigating whether oxidative stress in the brainstem caused by a maternal low-protein diet administered during a critical period of fetal/neonatal brain development (i.e during gestation and lactation) is affected by estradiol levels. Female Wistar rat offspring were divided into four groups according to their mothers' diets and to the serum estradiol levels of the offspring at the time of testing: (1) 22 days of age/control diet: (2) 22 days of age/low-protein diet; (3) 122 days of age/control diet: (4) 122 days of age/low-protein diet. Undernutrition in the context of low serum estradiol compared to undernutrition in a higher estradiol context resulted in increased levels of oxidative stress biomarkers and a reduction in enzymatic and non-enzymatic antioxidant defenses. Total global oxy-score showed oxidative damage in 22-day-old rats whose mothers had received a low-protein diet. In the 122-day-old group, we observed a decrease in oxidative stress biomarkers, increased enzymatic antioxidant activity, and a positive oxy-score when compared to control. We conclude from these results that following a protein deficiency in the maternal diet during early development of the offspring, estrogens present at high levels at reproductive age may confer resistance to the oxidative damage in the brainstem that is very apparent in pre-pubertal rats.

Several studies have shown that maternal low-protein (LP) diet induces detrimental effects in cardiovascular system and oxidative stress in male animals. Additional studies suggested that female has lower incidence of cardiovascular disease. However until present data, the possible effects of estradiol on the undernutrition during gestational and lactation periods are not discussed. The present study was conducted to evaluate the effects of a maternal LP diet during gestational and lactation period on oxidative balance in the female rat hearts ventricles at two ages. Dams were fed with normal protein (NP) or a LP diet during the gestational and lactation period, and their female offspring were divided into age groups (22 or 122 days, corresponding to a low or high estrogen level) composing four experimental groups. Evaluating the nutritional effect showed an increase in oxidative stress biomarkers and decrease in enzymatic defense in LP-22D compared with NP-22D. In contrast, no changes were observed in malondialdehyde and carbonyls, but an increase in glutathione-S-transferase (GST) activity in the LP-122D compared with NP-122D. The global oxy-score in the LP-22D group indicated a predominance of oxidative damage when compared with NP-22D, while in LP-122D group the global oxy-score was restored to NP-122D levels. Evaluating the estradiol effect, our data show a significant decrease in oxidative stress with increase in CAT and GST activity, associated with increase in intracellular thiols. Our data suggest that in situation with low levels of estradiol, hypoproteic diet during gestation and lactation period has detrimental effects on heart, however when estradiol levels raise, the detrimental effects induced are mitigated.

Previous studies showed that moderate exercise in adult rats enhances neutrophil function, although no studies were performed in juvenile rats. We evaluated the effects of moderate exercise on the neutrophil function in juvenile rats. Viability and neutrophils function were evaluated. Moderate exercise did not impair the viability and mitochondrial transmembrane potential of neutrophils, whereas there was greater reactive oxygen species production (164%; p < 0.001) and phagocytic capacity (29%; p < 0.05). Our results suggest that moderate exercise in juvenile rats improves neutrophil function, similar to adults.

There is a growing interest to better understand how lifestyle choices can improve memory functions. Treadmill exercise and long-chain n-3 polyunsaturated fatty acids found in fish oil are able to stimulate hippocampal antioxidant defenses and improve memory. The aim was to test whether fish oil and exercise can improve rat's performance on memory tasks and optimize hippocampal antioxidant state in an age-dependent manner. Therefore, young and adult rats were exercised and received fish oil during 4 weeks. The exercise was performed for 30 min/day, with the speed gradually increasing from the first to the last week. Afterwards, episodic memory was measured by the recognition of object identity and spatial location. Hippocampal oxidative state was investigated with the levels of malondialdehyde (MDA), carbonyls content, antioxidant enzymatic activity (superoxide dismutase (SOD), catalase (CAT)), and antioxidant nonenzymatic activity (reduced glutathione, sulfhydryl content). The adult rats treated with fish oil and exercise (FO&EX) were able to recognize object's shape and placement; however, FO&EX young rats had impaired spatial recognition (p < 0.05). The FO&EX young rats did not have reduced MDA or carbonyl content, though either fish oil or exercise reduced MDA (p < 0.05) and carbonyl levels (p < 0.01). Exercise increased SOD (p < 0.001) and CAT activities (p < 0.05), and fish oil enhanced SOD activity (p < 0.05) in young rats. At adulthood, exercise increased MDA levels (p < 0.05), and FO&EX reduced MDA (p < 0.001). Finally, exercise and fish oil improved nonenzymatic antioxidant defense (p < 0.05) only in adult rats. Results support age-dependent effects of fish oil and exercise on memory and oxidative state of the hippocampus during either neurodevelopment or adulthood.

It is well known that aging process alters cardiac physiology and the energy metabolism.Reactive oxygen species (ROS) are considered a key factor in the heart aging process. It has been demonstrated that activity of antioxidant systems are modified in aging and consequent weak resistance to ROS accumulation. Studies suggest that exercises ameliorate the process induced by aging. Therefore, the aim of the present study was to evaluate the long‐lasting effects of physical training during the period of critical brain development (i.e 15 ‐ 45 days of age) on oxidative balance in elderly hearts (585 days of age). The treadmill exercise of the rats was performed as previously described (Batista‐de‐Oliveira et al.Experim. Gerontol. 47:452–457). Malondialdehyde‐MDA formation was measured as described by Buege & Aust (Methods Enzymol 52, 302‐310), Carbonyl content as described by Levine et al. (Methods Enzymol 233:346‐57), GSH levels by Hissin & Hilf (Analytical Biochemistry 74:214‐216), SOD activity by Misra & Fridovich (JBC 247(10): 3170‐3175), Catalase‐CAT measured as described by Aebi (Methods Enzymol 105, 121‐126; 1984), and GST by Nascimento et al. (APNM 39:1‐8). Exercise increases MDA formation (75%); increases activity of SOD (24%) and it has no effects in additional enzymes. Our data suggest that submitting young rats to this protocol of moderate exercise does lead to long‐lasting impairment of oxidative balance in the hearts of aged rats.