Background: During the past decade a large number of reports described the roles of active oxygen species in the development or exacerbation of various kinds of diseases. The systemic antioxidant defense system often fails to control the excess free radicals. Such a condition necessitates external antioxidant supplementation either in the form of drugs or vitamins. Quantitative structure–activity relationship (QSAR) serves as an effective computational tool for search and design of active molecules that may eventually be synthesized and assayed. Objective/method: This review presents the current knowledge about QSAR studies of diverse groups of molecules with free radical scavenging activity. The QSAR studies summarized here would help to understand the proper mechanism underlying the interaction between the free radicals and antioxidant molecules. Conclusion: The primary determinant factors for potent antioxidant activity include the electronic distribution of the molecules together with their lipophilic...

Advances in quantitative structure-activity relationship models of antioxidants.

Insulin, a pancreatic hormone, is best known for its peripheral effects on the metabolism of glucose, fats and proteins. There is a growing body of evidence linking insulin action in the brain to neurodegenerative diseases. Insulin present in central nervous system is a regulator of central glucose metabolism nevertheless this glucoregulation is not the main function of insulin in the brain. Brain is known to be specifically vulnerable to oxidative products relative to other organs and altered brain insulin signaling may cause or promote neurodegenerative diseases which invalidates and reduces the quality of life. Insulin located within the brain is mostly of pancreatic origin or is produced in the brain itself crosses the blood-brain barrier and enters the brain via a receptor-mediated active transport system. Brain Insulin, insulin receptor and insulin receptor substrate-mediated signaling pathways play important roles in the regulation of peripheral metabolism, feeding behavior, memory and maintenance of neural functions such as neuronal growth and differentiation, neuromodulation and neuroprotection. In the present review, we would like to summarize the novel biological and pathophysiological roles of neuronal insulin in neurodegenerative diseases and describe the main signaling pathways in use for therapeutic strategies in the use of insulin to the cerebral tissues and their biological applications to neurodegenerative diseases.

Mechanisms of action of brain insulin against neurodegenerative diseases

The antioxidant enzyme extracellular superoxide dismutase (EC-SOD) is abundant in the lung and limits inflammation and tissue injury in response to many pulmonary insults. Previous studies reported a loss of full-length EC-SOD from the lung parenchyma with accumulation of proteolyzed EC-SOD in the airspace after interstitial lung injury. However, following airspace only inflammation (pneumonia), EC-SOD accumulates in the airspace without a loss from the interstitium, suggesting this antioxidant may be released from an extrapulmonary source.Because leukocytes are known to express EC-SOD and are prevalent in the bronchoalveolarlavage fluid after injury, it was hypothesized that these cells may transport and release EC-SODinto airspaces. To investigate this, bone marrow chimeras were generated using wild-type andEC-SOD knockout (KO) mice. Following intratracheal treatment with asbestos, reconstituted mice without pulmonary EC-SOD expression, but with EC-SOD in infiltrating and resident leukocytes did not have detectable levels of EC-SOD in the airspaces. In addition, leukocytederived EC-SOD did not significantly lessen inflammation or early stage fibrosis.Although these results indicate that leukocyte-derived EC-SOD is not influential in asbestos-induced interstitial lung injury, EC-SOD in these cells may play a role in attenuating pneumonias and other inflammatory diseases. To test this hypothesis, wild-type and EC-SOD KO mice were given Escherichia coli pneumonia. Notably, even though EC-SOD KO mice had greater pulmonary inflammation than wild-type mice, there was less bacterial clearance from their lungs following infection. While EC-SOD expression has been previously reported in macrophages and neutrophils, its function and subcellular localization in these inflammatory cells is unclear. In this study, EC-SOD was found to be in membrane bound vesicles of phagocytes. This finding led to the hypothesis that inflammatory cell EC-SOD may play a role in antibacterial defense. To investigate this, phagocytes from wild-type and EC-SOD KO mice were evaluated. While macrophages lacking EC-SOD produced more oxidants than EC-SOD expressing cells after stimulation, they had significantly impaired phagocytosis and bacterial killing ability. Overall, these studies suggest that while EC-SOD inside leukocytes does not contribute to interstitial lung injuries, it plays a central role in mediating bacterial infections by facilitating bacterial clearance and limiting inflammation by promoting phagocytosis.

/pdf/leukocyte-derived-extracellular-superoxide-dismutase-in-4o5q2py01f.pdf

Leukocyte-derived extracellular superoxide dismutase in pulmonary disease

Reactive Oxygen/Nitrogen Species: Generation and Reactions in the Lung

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Reactive Oxygen/Nitrogen Species: Generation and Reactions in the Lung