P602Sex-dependent perinatal alterations in plasma oxidative status in a rat model of fetal programming of hypertension

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Purpose. Adverse intrauterine growth induced by maternal undernutrition during pregnancy (MUN) is associated with low birth weight of the offspring and later development of hypertension. This process, known as fetal programming, has less impact on female offspring, which exhibit lower levels of blood pressure in adult life compared to males. Given the role of oxidative stress in the development of cardiovascular diseases we aimed to asses if fetal programming induces perinatal alterations in oxidative-antioxidant balance and the possible differences between males and females.

Methods. Sprague Dawley rats were used. Control (C) dams were fed ad libitum during pregnancy and lactation. MUN dams were fed 50% of the calculated ad libitum daily intake during the second half of gestation and returned to ad libitum diet during lactation. Offspring from both groups was standardized to 12 pups/litter (6 males and 6 females) and the rats were used at weaning (21 days). The rats were weighted at birth and at weaning. A blood sample was obtained by cardiac puncture at day 21 and the following parameters were measured in plasma: protein carbonyls, thiols, glutathion (spectrophotometric methods); total antioxidant capacity (TAC) and superoxide anion scavenging activity (SOSA) (luminometer) and catalase activity (Amplex red, fluorescence).

Results. Compared to C offspring, MUN rats exhibited a reduced weight at birth and at weaning. The weight difference was similar in males and females. Male MUN rats showed: 1) reduced plasma thiols, glutation, and SOSA levels; 2) increased carbonyl levels and 3) no differences in TAC and catalase activity. Female MUN rats showed no differences in any of the parameters measured, compared to female control rats.

Conclusions. These data suggest that fetal stress induced by maternal undernutrition in pregnancy affects the oxidative status at an early stage of development with a sex-dependent pattern. The lower level of plasma antioxidants in male offspring is likely to contribute to the higher level of hypertension developed by males compared to females in adult life.

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