Alterations in the expression of the apurinic/apyrimidinic endonuclease-1/redox factor-1 (APE/ref-1) and DNA damage in the caudal region of acute and chronic spinal cord injured rats treated by embryonic neural stem cells.

The oxidative mechanisms of injury-induced damage of neurons within the spinal cord are not very well understood. We used a model of T8-T9 spinal cord injury (SCI) in the rat to induce neuronal degeneration. In this spinal cord injury model, unilateral avulsion of the spinal cord causes oxidative stress of neurons. We tested the hypothesis that apurinic/apyrimidinic endonuclease (or redox effector factor-1, APE/Ref-1) regulates this neuronal oxidation mechanism in the spinal cord region caudal to the lesion, and that DNA damage is an early upstream signal. The embryonic neural stem cell therapy significantly decreased DNA-damage levels in both study groups - acutely (followed up to 7 days after SCI), and chronically (followed up to 28 days after SCI) injured animals. Meanwhile, mRNA levels of APE/Ref-1 significantly increased after embryonic neural stem cell therapy in acutely and chronically injured animals when compared to acute and chronic sham groups. Our data has demonstrated that an increase of APE/Ref-1 mRNA levels in the caudal region of spinal cord strongly correlated with DNA damage after traumatic spinal cord injury. We suggest that DNA damage can be observed both in lesional and caudal regions of the acutely and chronically injured groups, but DNA damage is reduced with embryonic neural stem cell therapy.

Effect of heat stress on oxidative stress, lipid peroxidation and some stress parameters in broilers.

1. This study was conducted to determine the effects of heat stress on fearfulness, leucocyte components, oxidative stress and lipid peroxidation in two commercial broiler strains, Cobb (C) and Ross (R). 2. At 36 and 37 d of age birds were exposed to 38 +/- 1 degree C for 3 h. Rectal temperatures, duration of tonic immobility (TI), haematocrit values, proportions of leucocyte components (heterophil, lymphocyte, basophil, eosinophil, monocyte), malondialdehyde (MDA) concentrations and antioxidant enzyme activities (CAT, SOD, GPx) of all the birds were determined, before and after heat treatment. 3. Rectal temperatures increased and haematocrit values decreased in birds exposed to heat stress. Heat stress caused a significant increase in heterophil/lymphocyte and in basophil ratios. 4. Exposing birds to heat stress increased duration of TI, suggesting heat-stressed birds tended to be more fearful. 5. Heat stress resulted in a significant Genotype x Treatment interaction for MDA concentration. CAT, SOD and GPx activities; MDA concentrations in heat-stressed R strain birds were greater than in heat-stressed C strain birds.

Effects of heat stress on growth, some blood variables and lipid oxidation in broilers exposed to high temperature at an early age.

1. This study was conducted to determine metabolic and physiological responses of 2 commercial broiler strains, Hubbard (H) and Cobb (C), exposed to an ambient temperature of 38 degrees +/- 1 degree C for 2 h at 14 and 15 d of age. 2. Exposure to high temperature at an early age resulted in weight loss in strain C, which was not compensated for by 35 d of age but there was no weight loss in strain H. 3. Exposure of broilers to heat stress (38 degrees +/- 1 degree C) at 35 d of age resulted in an increase in rectal temperature, regardless of previously high temperature experience but acid-base balance and haematocrit values were not affected by heat stress. 4. Malondialdehyde concentration was higher in unexposed birds than in previously exposed ones and did not significantly differ between strains.