Zeaxanthin-Biofortified Popcorn for Eye Health

Zeaxanthin is one of only two dietary carotenoids accumulated in the human macula. A key role of zeaxanthin is to protect the eyes’ photoreceptors from damage induced by blue light. Photoreceptor damage can lead to macular degeneration, which is the leading cause of blindness in Australia. Unfortunately, zeaxanthin is fairly rare in our diet. Popcorn (Zea mays var. everta) is a good dietary source of zeaxanthin, but the creation of zeaxanthin-biofortified popcorn potentially allows less popcorn to be consumed for an increased dietary dose of zeaxanthin. As zeaxanthin is an orange pigment, breeding for zeaxanthin gives popped kernels a naturally buttery colour, unlike standard popcorn, which is virtually white. The creation of naturally buttery-coloured popcorn potentially negates the practise of adding artificial butter-colourants, while also providing an excellent source of dietary zeaxanthin. The action of popping involves a combination of high-temperature and high-pressure, sufficient enough for starch to liquefy, and for the tiny beads of moisture within starch bodies to reach an extremely high pressure. Eventually, the kernel pericarp can no longer withstand this pressure, and an explosion occurs, resulting in butterfly-shaped popcorn. These extreme conditions, however, lead to an approximate 50% decline in zeaxanthin concentration following popping, and a gradual further 25% reduction over the next 24 h. Consequently, in order to optimise zeaxanthin intake, popcorn should be eaten as soon as possible after popping. Zeaxanthin-biofortified popcorn provides an additional dietary source of zeaxanthin, potentially reaching a sector of the community more prone to low zeaxanthin intake.

Role of TGF-Beta1/SMAD2/3 Pathway in Retinal Outer Deep Vascular Plexus and Photoreceptor Damage in Rat 50/10 Oxygen-Induced Retinopathy

In retinopathy of prematurity (ROP), outer deep vascular plexus (oDVP) was the emerging field, and the mechanisms of photoreceptor dysfunction remained to be explored. ODVP and photoreceptors were related, with oDVP being part of the supplier of oxygen and nutrients to photoreceptors, while their possible relationship in ROP was not clear. TGF-beta1 has been reported indispensable in oDVP development and altered in ROP patients and animal models. We hypothesized that the TGF-beta1 alteration in rat 50/10 oxygen-induced retinopathy (OIR) model contributed to oDVP malformation and exerted consequent effects on photoreceptor development. We first explored the profile of oDVP development in rat after birth and compared the expression of TGF-beta1 and pSMAD2/3 in Normoxia and OIR groups. Afterwards, the inhibitor of the pathway, LY364947, was used to establish the OIR, OIR+LY364947, Normoxia, and Normoxia+LY364947 groups. The oDVP and photoreceptor were examined by Isolectin B4 staining, western-blot of CD31 and Rho, and electron microscopy. ODVP sprouted at postnatal day 10 (D10) and reached the edge of retina at D14. The TGF-beta1/SMAD2/3 pathway was compromised during the critical period of oDVP development. The inhibitor simulated the oDVP retardation, pericyte, and photoreceptor malformation in the Normoxia+LY364947 group and might further compromise the development of oDVP and photoreceptor in the OIR+LY364947 group. The inhibition of the TGF-beta1/SMAD2/3 pathway indicated its critical role in oDVP malformation and photoreceptor damage, suggesting a possible therapeutic target of ROP treatment.