The effects of long-term dietary administration of corticosterone (CORT) on the induction of oxidative injury in broiler chickens (Gallus gallus domesticus) were evaluated. The experimental broiler chickens were fed with a diet supplemented with 30 mg CORT/kg diet for 2 weeks from 14 days of age onwards, while control chickens continued to consume the control diet. The growth performance parameters were recorded weekly, and a blood sample was obtained from eight birds of both groups before CORT administration and at 3, 7 and 14 days after treatment. The results showed that chronic CORT administration resulted in enhanced proteolysis and gluconeogenesis. Furthermore, CORT administration may initially induce the formation of reactive oxygen species (ROS) as indirectly reflected by an increase in lipid peroxidation. However, the significantly increased plasma uric acid (UA) and ceruloplasmin (CP) levels after 3 days of treatment indicates an enhancement of the nonenzymatic antioxidant capacity during stress, and in this way, the development of a more severe oxidative injury is alleviated. Broiler chickens seem to adapt to high circulating CORT levels in terms of their redox homeostasis after 3 days of treatment under the present experimental conditions.

Oxidative stress induced by corticosterone administration in broiler chickens (Gallus gallus domesticus) 1. Chronic exposure.

Glucocorticoids in osteonecrosis of the femoral head: A new understanding of the mechanisms of action

Two trials were conducted to evaluate the effects of short-term administration of corticosterone (CORT) on the induction of oxidative injury in broiler chickens (Gallus gallus domesticus). Twelve broiler chickens of 30 and of 40 days of age were respectively employed in Trial 1 and 2. Half of the chickens were administered subcutaneously with CORT (4 mg/kg body weight [BW] in corn oil), while another half served as controls (corn oil) in each trail. In Trial 1, a blood sample was obtained from each chicken immediately before administration and at 1 and 3 h after injection. In Trial 2, the liver and heart were obtained after 3 h of CORT exposure. Short-term administration of CORT resulted in enhanced proteolysis and gluconeogenesis. There were no obvious changes in lipid peroxidation status of the heart and liver, whereas a decrease in lipid peroxidation in the plasma was observed after acute CORT exposure. The significantly increased plasma nonenzymatic antioxidants (uric acid [UA] and total antioxidant capacity) in concert with the enhanced enzymatic antioxidant activity (SOD in heart) during short-term CORT administration indicate preventive changes to counteract the oxidative injury, and these may be tissue specific.

Oxidative stress induced by corticosterone administration in broiler chickens (Gallus gallus domesticus) 2. Short-term effect.

Effects of trophic exposure to dexamethasone and diclofenac in freshwater fish

The blood pressure-raising effects of adrenocortical steroids with predominantly glucocorticoid activity, both naturally occurring and synthetic, are well known. Recent evidence suggests that the nitric oxide system plays a key role in the hypertension produced by glucocorticoids. Glucocorticoid actions at various sites in the nitric oxide synthase (NOS) pathway may result in elevated blood pressure. These include: alterations in l-arginine availability or transport; NOS2 and NOS3 downregulation; reduced cofactor bioavailability; NOS uncoupling; a concomitant elevation in reactive oxygen species and removal of nitric oxide (NO) from the vascular environment; alterations in whole body antioxidant status; and erythropoietin induced resistance to NO.

The nitric oxide system in glucocorticoid-induced hypertension.

This study was designed to investigate the alterations in thiobarbituric acid reactants (TBA-reactants) and enzymatic and nonenzymatic antioxidant levels induced by dexamethasone (Dex) in heart and kidney and to find out whether these alterations induced by Dex and its hypertensive effect had any role in the maintenance of hypertension in this model. Administration of dexamethasone induced severe loss of body weight, significant increase in heart and kidney weights and also marked electrocardiographic changes. The protein content in heart and kidney increased significantly during Dex administration and returned to near normalcy after withdrawal. Total activity of lactate dehydrogenase showed a significant increase in heart till day 8 of treatment, whereas in serum, it exhibited a significant decrease. The activity of CK in heart showed an increase till day 8 of treatment and approached normalcy thereafter. In serum, CK exhibited a decrease till day 8, remaining insignificant thereafter. CKMB in heart showed an insignificant increase initially, reaching normal levels on Dex withdrawal, whereas in serum, it showed a significant decrease throughout the experimental period. Mean arterial pressure (MAP) and heart rate increased significantly, while a significant elevation in the ST segment was noticed during administration as well as after withdrawal of dex. The TBA-reactants levels were found to increase in heart and kidney during days 12 and 16 of administration with Dex and even after withdrawal of Dex, the levels were insignificantly elevated. The level of glutathione in heart and kidney increased from day 4 onwards and reached normalcy during the later stages of treatment and after withdrawal of Dex. The total sulfhydryl groups exhibited a significant increase in both heart and kidney throughout the experiment. The antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and glutathione S-transferase exhibited a significant decrease in heart during Dex administration whereas, in kidney, they exhibited a significant increase during treatment and after withdrawal of Dex. Thus, Dex induced rise in mean arterial pressure, significant alterations in electrocardiographic parameters and also marked alterations in enzymatic and nonenzymatic antioxidant levels and in the TBA-reactants level in heart and kidney.

Sampath Rajashree

Papers

Dexamethasone induced alterations in enzymatic and nonenzymatic antioxidant status in heart and kidney of rats.