Faculty Opinions recommendation of Developmental programming of cardiovascular dysfunction by prenatal hypoxia and oxidative stress.

Hypoxia is a common form of intrauterine stress characterized by exposure to low oxygen concentrations. Gestational hypoxia is associated with the generation of reactive oxygen species. Increase in oxidative stress is responsible for damage to proteins, lipids and DNA with consequent impairment of normal cellular functions. The purpose of this review is to propose a summary of preclinical and clinical evidences designed to outline the correlation between fetal hypoxia and oxidative stress. The results of the studies described show that increases of oxidative stress in the placenta is responsible for changes in fetal development. Specifically, oxidative stress plays a key role in vascular, cardiac and neurological disease and reproductive function dysfunctions. Moreover, the different finding suggests that the prenatal hypoxia-induced oxidative stress is associated with pregnancy complications, responsible for changes in fetal programming. In this way, fetal hypoxia predisposes the offspring to congenital anomalies and chronic diseases in future life. Several antioxidant agents, such as melatonin, erythropoietin, vitamin C, resveratrol and hydrogen, shown potential protective effects in prenatal hypoxia. However, future investigations will be needed to allow the implementation of these antioxidants in clinical practice for the promotion of health in early intrauterine life, in fetuses and children.

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Diabetes, Developmental Programming and Oxidative Stress

The Molecular Basis for the Link between Maternal Health and the Origin of Fetal Congenital Abnormalities: An Overview of Association with Oxidative Stress ◽

10.2174/978160805286811101010116 ◽

2012 ◽

pp. 116-126

Keyword(s):

Oxidative Stress ◽

Developmental Programming ◽

And Oxidative Stress

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Early life experience contributes to the developmental programming of depressive-like behaviour, neuroinflammation and oxidative stress

Journal of Psychiatric Research ◽

10.1016/j.jpsychires.2017.08.020 ◽

2017 ◽

Vol 95 ◽

pp. 196-207 ◽

Cited By ~ 23

Author(s):

Gislaine Z. Réus ◽

Gabrielly C. Fernandes ◽

Airam B. de Moura ◽

Ritele H. Silva ◽

Ana Caroline Darabas ◽

...

Keyword(s):

Oxidative Stress ◽

Early Life ◽

Life Experience ◽

Developmental Programming ◽

Early Life Experience ◽

And Oxidative Stress

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Prenatal hypoxia, habituation memory and oxidative stress

Pharmacology Biochemistry and Behavior ◽

10.1016/j.pbb.2013.04.004 ◽

2013 ◽

Vol 107 ◽

pp. 24-28 ◽

Cited By ~ 13

Author(s):

I.M. Sab ◽

M.M.D. Ferraz ◽

T.A.S. Amaral ◽

A.C. Resende ◽

M.R. Ferraz ◽

...

Keyword(s):

Oxidative Stress ◽

Prenatal Hypoxia ◽

And Oxidative Stress

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Chemotherapeutic-Induced Cardiovascular Dysfunction: Physiological Effects, Early Detection—The Role of Telomerase to Counteract Mitochondrial Defects and Oxidative Stress

International Journal of Molecular Sciences ◽

10.3390/ijms19030797 ◽

2018 ◽

Vol 19 (3) ◽

pp. 797 ◽

Cited By ~ 4

Author(s):

Nabeel Quryshi ◽

Laura Norwood Toro ◽

Karima Ait-Aissa ◽

Amanda Kong ◽

Andreas Beyer

Keyword(s):

Oxidative Stress ◽

Early Detection ◽

Physiological Effects ◽

Cardiovascular Dysfunction ◽

Mitochondrial Defects ◽

And Oxidative Stress

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Abstract 135: Obesity Accelerates the Deterioration of Renal Function in Developmental Programming of Hypertension. Role of Angiotensin Ii and Oxidative Stress

Hypertension ◽

10.1161/hyp.68.suppl_1.135 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Antonio Tapia ◽

Juan M Moreno ◽

Maria T Llinas ◽

F. Javier Salazar

Keyword(s):

Oxidative Stress ◽

Renal Function ◽

Angiotensin Ii ◽

Perinatal Period ◽

Developmental Programming ◽

Ang Ii ◽

Obese Rats ◽

Renal Vascular ◽

And Oxidative Stress

Numerous studies have shown gender-dependent differences in the deterioration of renal function in models of developmental programming of hypertension (DPH). It is also known that obesity is associated to changes in renal function and that both angiotensin II (Ang II) and oxidative stress are involved in the renal alterations that occur in obesity and in animals with DPH. The main objectives were to examine whether the increment of arterial pressure (AP) and the deterioration of renal function are accelerated as a consequence of obesity in SD rats with DPH; whether these changes are gender-dependent; and to evaluate the role of Ang II and oxidative stress in these AP and renal function changes. A high fat diet (60%) was given during the first 4 months of age and DPH was induced by an AT receptor antagonist during nephrogenic period (ARAnp). Systolic AP (mmHg) was greater (P<0.05) in ARAnp-obese rats (167 ± 3 in ♂; 146 ± 4 in ♀) than in ARAnp (155 ± 3 in ♂; 137 ± 3 in ♀); obese (147 ± 2 in ♂; 137 ± 2 in ♀) or control (127 ± 1 in ♂; 119 ± 2 in ♀) rats. Three days administration of candesartan (7 mg/kg/day) led to a decrease in AP that was greater (P<0.05) in ARAnp-obese rats (55 ± 3 in ♂; 45 ± 4 in ♀) than in ARAnp (40 ± 3 in ♂; 37 ± 4 in ♀); obese (38 ± 4 in ♂; 27 ± 4 in ♀) or control (12 ± 2 in ♂; 14 ± 3 in ♀) rats. The acute Ang II infusion (30 ng/kg/min) induced an increase in renal vascular resistance (mmHg/ml/min/gr kw) that was also greater in ARAnp-obese rats (217 ± 45% in ♂; 145 ± 38% in ♀) than in ARAnp (103 ± 9% in ♂; 97 ± 8% in ♀); obese (106 ± 14% in ♂; 106 ± 17 in ♀) or control (51 ± 7% in ♂; 51 ± 10% in ♀) rats. The response to candesartan or Ang II infusion in ARAnp-obese rats was gender-dependent and may be explained by an enhanced oxidative stress. The expression of P67phox in the renal cortex was greater (P<0.05) in ARAnp-obese rats (3,00 ± 0,05 in ♂; 2,60 ± 0,04 in ♀) than in ARAnp (1,16 ± 0,04 in ♂; 1,66 ± 0,03 in ♀); obese (0,94 ± 0,06 in ♂; 1,02 ± 0,02 in ♀) or control (1,00 ± 0,02 in ♂; 1,02 ± 0,023 in ♀) rats. The results of this study suggest that obesity at an early age enhances the hypertension and accelerates the deterioration of renal function that occurs when cardiovascular disease is programmed during the perinatal period. It is also shown that Ang II and oxidative stress seems to play an important role in these AP and renal function changes.

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