Erythrocyte osmotic fragility and general health status of adolescent Sprague Dawley rats supplemented with Hibiscus sabdariffa aqueous calyx extracts as neonates followed by a high‐fructose diet post‐weaning

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Erythrocytes, in performing their major function of transporting oxygen and carbon dioxide between the lungs and the tissues (Ambali et al., 2011), are exposed to oxidative damage as a result of the formation of reactive oxygen species (ROS) due to high oxygen partial pressure in the lungs (Hatherill et al., 1991). The erythrocytes also have an abundance of polyunsaturated fatty acids (PUFA) in their cell membranes and a rich iron content in their haemoglobin further increasing their susceptibility to peroxidative damage (Hatherill et al., 1991). The ionic Fe2+ in the haemoglobin functions as a catalyst in lipid peroxidation leading to the formation of malondialdehyde (MDA) (Mohamed et al., 2013). However, the erythrocytes have an effective antioxidant enzyme system that protects them from consequences of perpetual exposure to ROS (Rai et al., 2009). These antioxidant enzymes include superoxide dismutase, catalase and glutathione S‐transferase (Rai et al., 2009).
5The rise in incidence of metabolic syndrome has been linked to changes in dietary habits and reduced physical exercise (Armitage et al., 2004). Due to its sweetness and affordability, high‐fructose corn syrup is found in many processed foods (Angelova and Boyadjiev, 2013). Consumption of a diet high in fructose causes disturbances in lipid metabolism leading to increased lipogenesis (Kelley et al., 2004) and formation of lipid peroxides that are associated with increased erythrocyte membrane damage (Ambali et al., 2010). When spontaneously hypertensive rats were fed a high‐fructose diet (60%, w/w), a lower antioxidant capacity was observed manifesting as a reduction in copper/zinc SOD and glutathione peroxidase activities when compared to the control group which received a starch diet (Girard et al., 2006).
Epidemiological and clinical evidence further suggests a link between nutritional and stressful events in the perinatal environment and the manifestation of metabolic diseases in adult life (Osmond et al., 1993; Hales and Barker, 2001; Gluckman and Hanson, 2004). This linkage is attributed to epigenetic changes that occur during the critical windows of relative tissue plasticity in the perinatal period, thereby affecting the expression or silencing of genes (Gallou‐Kabani and Junien, 2005). Thus, interventions/experiences in early life can programme disease susceptibility/development later in life when animals are exposed to the same primary intervention as experienced in early life or even in the absence of the experience later in life. The early intervention may thus confer protection or increase susceptibility to the development of disease.
Hibiscus sabdariffa (HS) is a plant of the Malvaceae family, and it is consumed widely by all age groups for medicinal and recreational purposes (Da‐Costa‐Rocha et al., 2014; Patel, 2014). It has an abundance of antioxidants (Farombi and Fakoya, 2005; Usoh et al., 2005; Hirunpanich et al., 2006), which have been found to decrease the levels of lipid peroxidation by‐products also known as thiobarbituric acid‐reactive substances (TBARS). Increased levels of TBARS are usually associated with high‐fructose feeding (Miatello et al., 2005). HS aqueous extracts were also found to have protective effects against erythrocyte membrane oxidative damage in streptozotocin‐induced diabetic rats (Mohamed et al., 2013).
HS aqueous extracts were shown to increase body mass index and delay onset of puberty in female rats when consumed in the post‐weaning period (Iyare and Adegoke, 2008) and in growing pups whose dams were fed with HS extracts during lactation (Iyare and Nwagha, 2009). Therefore, in this study, we aimed to find out whether the administration of HS aqueous calyx extracts to rats in the neonatal period would have an effect on their erythrocyte osmotic fragility and general health following the intake of a high‐fructose diet post‐weaning.
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