Abstract
Prolonged hyperglycemia is one of the main causes of reactive oxygen species and free radicals generation in diabetes which may affect various organs, including the eye. Oxidative damage to proteins and lipids in the eye lens could lead to cataract formation. To cope with oxidative stress, the endogenous antioxidative system may be supported by the supplementation of exogenous antioxidants. The aim of this study was to evaluate the effect of chrysin, a natural flavonoid, on oxidative stress and polyol pathway-related markers in the lenses of streptozotocin-induced type 1 male diabetic rats. Chrysin at doses of 50 and 100 mg/kg was administered by gavage for 28 days. This treatment resulted in a decrease in antioxidative enzymes activity and oxidative stress index. Moreover, chrysin administration elevated the reduced glutathione level in the lenses. A decrease in the markers linked to oxidative damage to proteins and lipids in the lenses was noted, especially after treatment with 50 mg/kg of chrysin. Neither of the chrysin doses affected glycemia-related markers in the serum or altered parameters related to the polyol pathway and advanced glycation end-products level in the lenses of diabetic rats. Upon obtaining results, it can be concluded that chrysin reveals antioxidative activity in the lenses but shows no antihyperglycemic or antiglycation properties.
Highlights
The term “oxidative stress”, describing an oxidative damage to the cells or organs, was proposed in 1985 and was originally defined as “a disturbance in the prooxidant-antioxidant balance in favor of the former” [1]
In this study we demonstrated that chrysin administered by gavage for 28 days reduced oxidative stress in the lenses of the male type 1 diabetic rats by decreasing the activity of
In this study we demonstrated that chrysin administered by gavage for 28 days reduced oxidative antioxidative enzymes, reducing the levels of the oxidative damage markers and improving the stress in the lenses of the male type 1 diabetic rats by decreasing the activity of antioxidative enzymes, reducing the levels of the oxidative damage markers and improving the oxidative stress index
Summary
The term “oxidative stress”, describing an oxidative damage to the cells or organs, was proposed in 1985 and was originally defined as “a disturbance in the prooxidant-antioxidant balance in favor of the former” [1]. There are many types of prooxidants, such as free radicals or reactive oxygen species (ROS). Free radicals are particles with one or more unpaired electrons and ROS are reactive compounds containing oxygen. ROS are produced mainly in the mitochondrial respiratory chain. In smaller amounts they are generated in endoplasmic reticulum and peroxisomes, as well as during “respiratory burst” with involvement of the NADPH oxidase complex. ROS may arise from the autooxidation of endogenous particles such as epinephrine [3,5].
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