Neuroprotective agents effective against radiation damage of central nervous system.

Ionizing radiation caused by medical treatments, nuclear events or even space flights can irreversibly damage structure and function of brain cells. That can result in serious brain damage, with memory and behavior disorders, or even fatal oncologic or neurodegenerative illnesses. Currently used treatments and drugs are mostly targeting biochemical processes of cell apoptosis, radiation toxicity, neuroinflammation, and conditions such as cognitive-behavioral disturbances or others that result from the radiation insult.

Effects of low and high deprenyl dose on antioxidant enzyme activities in the adult rat brain.

We evaluated the effects of low dose deprenyl (LDD, 0.0025 mg/kg per day) and high dose deprenyl (HDD, 0.25 mg/kg per day) treatment of male Wistar rats for 30 days on the activities of SOD and CAT in the cortex, striatum, and hippocampus.

Neuroprotection and antioxidants.

Ischemia as a serious neurodegenerative disorder causes together with reperfusion injury many changes in nervous tissue. Most of the neuronal damage is caused by complex of biochemical reactions and substantial processes, such as protein agregation, reactions of free radicals, insufficient blood supply, glutamate excitotoxicity, and oxidative stress. The result of these processes can be apoptotic or necrotic cell death and it can lead to an irreversible damage.

Postconditioning Effectively Prevents Trimethyltin Induced Neuronal Damage in the Rat Brain.

Trimethyltin (TMT) is a toxic substance formerly used as a catalyst in the production of organic substances, as well as in industry and agriculture. TMT poisoning has caused death or severe injury in many dozens of people. The toxicity of TMT is mediated by dose dependent selective damage to the limbic system in humans and other animals, specifically the degeneration of CA1 neurons in the hippocampus.

Effect of Bradykinin Postconditioning on Ischemic and Toxic Brain Damage.

Brain damage caused by ischemia or toxic agents leads in selectively vulnerable regions to apoptosis-like delayed neuronal death and can result in irreversible damage. Selectively vulnerable neurons of the CA1 area of hippocampus are particularly sensitive to ischemic damage. We investigated the effects of bradykinin (BR) postconditioning on cerebral ischemic and toxic injury.