Co-Enzyme Q10 and n-3 Polyunsaturated Fatty Acid Supplementation Reverse Intermittent Hypoxia-Induced Growth Restriction and Improved Antioxidant Profiles in Neonatal Rats

Abstract

Neonatal intermittent hypoxia (IH) increases the risk for many morbidities in extremely low birth weight/gestational age (ELBW/ELGA) neonates with compromised antioxidant systems and poor growth. We hypothesized that supplementation with coenzyme Q10 (CoQ10, ubiquinol) or n-3 polyunsaturated fatty acids (PUFAs) during neonatal IH improves antioxidant profiles and somatic growth in neonatal rats. Newborn rats were exposed to two IH paradigms at birth (P0): (1) 50% O2 with brief hypoxic episodes (12% O2); or (2) room air (RA) with brief hypoxia, until P14 during which they received daily oral CoQ10 in olive oil, n-3 PUFAs in fish oil, or olive oil only from P0 to P14. Pups were studied at P14 or placed in RA until P21 for recovery from IH (IHR). Body weight and length; organ weights; and serum antioxidants and growth factors were determined at P14 and P21. Neonatal IH resulted in sustained reductions in somatic growth, an effect that was reversed with n-3 PUFAs. Improved growth was associated with higher serum growth factors. CoQ10 decreased superoxide dismutase (SOD) and glutathione, but increased catalase, suggesting reduced oxidative stress. Further studies are needed to determine the synergistic effects of CoQ10 and n-3 PUFA co-administration for the prevention of IH-induced oxidative stress and postnatal growth deficits.

The Thiol-Disulfide Homeostasis and Coenzyme Q10 in Conjunction with Vitamin E Effect on Retinopathy Prematurity

“…CoQ10s have a high molecular weight and a lipophilic structure that is almost too strong to melt in an aqueous environment. Although there are studies suggesting that CoQ10 has poor bioavailability because it is not water-soluble, there are other studies that show its benefits many organs in the body [11]. Its strong lipophilic structure limits its therapeutic value [23 -25].…”

“…Oxidative stress plays a critical role in retinal injury and the prognosis of ROP, diabetic retinopathy and ischaemic oxidative retinopathies, such as age-related macular degeneration (AMD); therefore, CoQ10 has an important role in all of these oxidative retinopathies [3]. In their recently published study, Beharry et al demonstrated that CoQ10 and n-3 PUFA supplementation in IH elicited protective effects against ROP [11]. CoQ10 reduced VEGF expression, maintained astrocytic integrity, reduced neovascularisation and normalised retinal layers.…”

“…Neonatal Intermittent Hypoxia (IH) is a recurrent, shortterm (<3 min) decrease in oxygen saturation [11]. IH episodes are typically a consequence of an immature respiratory control system, and may result in the disruption of the antioxidant system, particularly in premature infants, leading to increased retinal neovascularisation.…”

“…IH episodes are typically a consequence of an immature respiratory control system, and may result in the disruption of the antioxidant system, particularly in premature infants, leading to increased retinal neovascularisation. IH-induced mitochondrial ROS are toxic, causing lipid peroxidation and damaging cell membranes [11].…”

“…The antioxidant is a naturally-occurring compound, primarily playing a bioenergenetic role in the cell [12]. CoQ10 has been suggested to inhibit the developmental deficits caused by IH-induced oxidative stress [11].…”