Effect of Maternal and Post-weaning Nutrition on the Oxidative Systems of the Rat Lens

Abstract

Cataract or clouding of the lens can be caused by oxidative stress which damages lens fibre cell protein structure and reduces overall transparency and refractive ability. Low birth weight (for example, due to maternal undernutrition) has been associated with increased incidence of childhood cataract (SanGiovanni, Chew et al. 2002). Similarly, obesity, due to high fat diets post-weaning has been shown to increase age-related cataract (particularly following type-2 diabetes) (Congdon, Friedman et al. 2003). Based on these observations I have investigated the effect of control (C) or high-fat (HF) diets post-weaning on oxidative defence systems in different regions of rat lenses extracted from animals born to either normal (C) or undernourished (UN) mothers 160 days post birth. In all 4 groups (Control+Control; Control+HF; UN+Control; UN+HF) dark and bright field microscopy used to assess the clarity and refractive ability of the lenses revealed no lens opacification. The refractive ability was however, reduced mainly in male rats who underwent both maternal UN and a high fat post-weaning diet (UN+HF). Subsequently the lens cortical and core regions were separated and assays were carried out to measure total antioxidant capacity (TAC); glutathione (GSH; predominant antioxidant in the lens); oxidised glutathione (GSSG) and markers of oxidative stress malondialdehyde (MDA) and protein carbonyls (PCs) through several assays. This analysis revealed that maternal UN followed by a control diet post-weaning for 160 days did not cause any overall changes to the oxidative status of the lens. We believe that the control diet post-weaning may have compensated for the effect of maternal UN in the lens. When considering the effect of obesity, elevated MDA and PC in lenses of maternal control groups fed a high fat diet post-weaning was observed. The effect of obesity was also compounded by maternal UN with lower GSH levels and greater MDA and PC being expressed in both male and female offspring. Extending from previous studies it is possible that the hyperglycaemia (McCaleb and Sredy 1992, Shen, Zou et al. 2009), hyperleptinemia (Gómez-Ambrosi, Salvador et al. 2004) and increased adipose tissue resulting from a high-fat post-weaning diet (Furukawa, Fujita et al. 2004) caused greater oxidative stress within the lens at 160 days. In this study, we have shown that lens antioxidant defence systems following maternal undernutrition is adversely affected in the presence of a poor postnatal nutritional environment. This indicates an interaction between maternal and postnatal diet that contributes to the oxidative status of the lens.