File Name: oxidative stress in cancer aids and neurodegenerative diseases .zip
Skip to search form Skip to main content You are currently offline. Some features of the site may not work correctly. Pasquier Published Medicine. Interestingly, oxidative stress in cancer aids and neurodegenerative diseases that you really wait for now is coming. It's significant to wait for the representative and beneficial books to read. Every book that is provided in better way and utterance will be expected by many peoples.
Oxidatively damaged proteins accumulate with age in almost all cell types and tissues. The activity of chaperone-mediated autophagy CMA , a selective pathway for the degradation of cytosolic proteins in lysosomes, decreases with age. We have analyzed the possible participation of CMA in the removal of oxidized proteins in rat liver and cultured mouse fibroblasts. Added to the fact that CMA substrates, when oxidized, are more efficiently internalized into lysosomes, we have found a constitutive activation of CMA during oxidative stress. Oxidation-induced activation of CMA correlates with higher levels of several components of the lysosomal translocation complex, but in particular of the lumenal chaperone, required for substrate uptake, and of the lysosomal membrane protein lamp type 2a, previously identified as a receptor for this pathway. In contrast with the well characterized mechanism of CMA activation during nutritional stress, which does not require de novo synthesis of the receptor, oxidation-induced activation of CMA is attained through transcriptional up-regulation of lamp2a.
Free radicals are common outcome of normal aerobic cellular metabolism. In-built antioxidant system of body plays its decisive role in prevention of any loss due to free radicals. However, imbalanced defense mechanism of antioxidants, overproduction or incorporation of free radicals from environment to living system leads to serious penalty leading to neuro-degeneration. Neural cells suffer functional or sensory loss in neurodegenerative diseases. Apart from several other environmental or genetic factors, oxidative stress OS leading to free radical attack on neural cells contributes calamitous role to neuro-degeneration. Toxicity of free radicals contributes to proteins and DNA injury, inflammation, tissue damage and subsequent cellular apoptosis.
Materials and Methods: A total of 28 AD, 42 PD patients and 42 healthy controls aged yrs were recruited for the study. This indicates that reduced SOD plays a prominent role in the increase of OS in neuronal degeneration. This article has been cited by 1 Neuroprotective effect of Reinwardtia indica against scopolamine induced memory-impairment in rat by attenuating oxidative stress Prabhat Upadhyay,Rashmi Shukla,Kavindra Nath Tiwari,G. Tantisira,Ratchanee Rodsiri Phytomedicine. Carvalho,Michael Maes,Adam J. Walker,Basant K. Puri Behavioural Brain Research.
Typically in aerobic metabolism, organic compounds such as nucleic acids, proteins and lipids can undergo structural damage by oxidative reactions. Various diseases such as cancer, diabetes, cardiovascular diseases and neurodegenerative clearly exemplify the chronic oxidative stress. Therefore, it is important to consider that at low and moderate ROS levels, it can, for example, act as signaling molecules that support cell proliferation and differentiation and activate survival pathways in response to stress. Correlations between oxidative stress and disease should be carefully investigated in order to understand whether oxidative stress actually increases susceptibility to a particular disease or opposite. The generation of free radicals is a continuous physiological process, fulfilling relevant biological functions.
Alexander V. Ivanov, Birke Bartosch, Maria G. Viral, bacterial, and parasitic infections comprise a vast group of etiological agents that cause acute or chronic diseases. According to WHO, they represent one of the major causes of human morbidity and mortality.
Oxidative stress OS has the ability to damage different molecules and cellular structures, altering the correct function of organs and systems. OS accumulates in the body by endogenous and exogenous mechanisms. Increasing evidence points to the involvement of OS in the physiopathology of various chronic diseases that require prolonged periods of pharmacological treatment.
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