No abstract

One of the mechanisms proposed to explain lens opacification is the oxidation of crystallins, either by radiation or reactive oxygen species (ROS). It has been shown that melatonin has both an anti-peroxidative effect on several tissues and a scavenger effect on ROS. The purpose of this study was to determine the antioxidant role of melatonin (5 mg/kg/day) against radiation-induced cataract in the lens after total-cranium irradiation of rats with a single dose of 5 Gy. Sprague-Dawley rats were divided into four groups. Control group received neither melatonin nor irradiation. Irradiated rats (IR) and melatonin+irradiated rats (IR+Mel) groups were exposed to total cranium irradiation of 5 Gy in a single dose by using a cobalt-60 teletherapy unit. IR+Mel and melatonin (Mel) groups were administered 5 mg/kg melatonin daily by intraperitoneal injections during ten days. Chylack's cataract classification was used in this study. At the end of the 10th day, the rats were killed and their eyes were enucleated to measure the antioxidant enzymes i.e. the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and lipid peroxidation level (malondialdehyde (MDA)). Irradiation significantly increased the MDA level, as an end product of lipid peroxidation, and also significantly decreased SOD and GSH-Px activity, emphasizing the generation of increased oxidative stress. Rats injected with melatonin only did not cause cataract formation. Melatonin supplementation with irradiation significantly increased the activity of SOD and GSH-Px enzymes and significantly decreased the MDA level. Total cranium irradiation of 5 Gy in a single dose enhanced cataract formation, and melatonin supplementation protected the lenses from radiation-induced cataract formation. Our results suggest that supplementing cancer patients with adjuvant therapy of melatonin may reduce patients suffering from toxic therapeutic regimens such as chemotherapy and/or radiotherapy and may provide an alleviation of the symptoms due to radiation-induced organ injuries.

L-carnitine may protect against the damage produced by gamma radiation by increasing the activity of the SOD enzyme and by scavenging free radicals generated by ionizing radiation. As a result of this process, MDA as an indicator of lipid peroxidation may decrease.

Our aim was to determine the effects of vitamin E and L-carnitine supplementation, individually or in combination, on radiation-induced brain and retinal damages in a rat model. Group 1 received no treatment (control arm). Group 2 received a total dose of 15 Gy external radiotherapy (RT) to whole brain by Cobalt-60 teletherapy machine. Groups 3, 4, and 5 received irradiation plus 40 kg(-1) day(-1) Vitamin E or 200 mg kg(-1)day(-1) L-carnitine alone or in combination. Brain and retinal damages were histopathologically evaluated by two independent pathologists. Antioxidant enzyme levels were also measured. Radiation significantly increased brain and retinal damages. A significant increase in malondialdehyde levels as well as a decrease in superoxide dismutase and catalase enzymes in brain was found in group 2. Separate administration of Vitamin E+RT and L-carnitine+RT significantly reduced the severity of brain and retinal damages and decreased the malondialdehyde levels and increased the activity of superoxide dismutase and catalase enzymes in the brain. The findings of current study support the antioxidant and radioprotective roles of vitamin E and L-carnitine. However, the combined use of Vitamin E and L-carnitine plus irradiation interestingly did not exhibit an additive radioprotective effect.

We suggest that Ginkgo biloba is an antioxidant that protects the rat lens from radiation-induced cataracts.