Dr. Kara completed his doctorate in the Department of Histology and Embryology at the Faculty of Medicine in 2012. He worked as a lecturer in the Faculty of Veterinary Medicine, Department of Histology and Embryology, Atatürk University, Bingöl Universities, Turkey. Dr. Kara has authored and co-authored fifty-seven journal papers, four book chapters, and thirty other types of publications.
Various histopathological and cytopathological processes, such as inflammation, cell injury, tissue regeneration, hemodynamic disorders, and neoplasia, constitute important processes in the formation mechanism of many diseases. Molecular mechanisms are involved in the emergence of these basic pathological processes. Learning the organization from molecule to tissue guides investigating the mechanisms of many diseases. This book describes and discusses these pathological processes and their association with molecular mechanisms of the formation of various diseases.
Go to the bookFree radical production related with many stress factors including radiation, drugs, ageing and trauma plays a key role in cell death. Notwithstanding, free radicals can cause pathology in a variety of diseases through oxidative stress: Under oxidative stress, excessive production of free radicals can trigger cell death by primarily DNA and all cellular macromolecule damages. Also, excessive free radicals have a role in early inducers of autophagy cell death upon nutrient deprivation. Autophagy is physiologic process of eukaryotic systems, which have significant role in adaptation to oxidative stress by degradation of metalloproteins and oxidatively damaged macromolecules. By oxidizing, membrane injuries allow the leakage of enzymes and contribute to cell damage. However, recent publications demonstrate the protecting role of lysosome system during excessive reactive oxygen species (ROS) production by the elimination of damaged proteins or organelles. Activation of autophagic or lysosomal system can eliminate the oxidizing components of cell in oxidative stress response. This chapter aims to provide the novel insight data for oxidative damage-mediated autophagy as well as their metabolic networks.
Part of the book: Free Radicals and Diseases
Melatonin is an endocrine product released from the gland known as the pineal gland and is predominantly secreted during the night. Light exerts an inhibitory effect on melatonin secretion in the pineal gland. The suprachiasmatic nucleus controls pineal melatonin synthesis and its release via the peripheral sympathetic nervous system, which includes synapses in the intermediolateral cell column of the thoracic cord and its projection toward the superior cervical ganglia. Melatonin regulates many physiological functions in the body through membrane receptors and nuclear binding sites. In a chick study, the presence of melatonin receptors in cardiomyocytes was reported and, in another study, MT1 and MT2 membrane receptors were identified in left ventricular cardiomyocytes of the human heart. For this reason, it is suggested that melatonin has some regulatory effects on the cardiovascular system. Ischemic heart disease and myocardial infarctions are the main cause of cardiovascular death. Studies have shown that melatonin applications reduce the amount of blood cholesterol, LDL, and triglyceride and increase the amount of HDL. In light of these data, it can be said that melatonin is an important cardiovascular system protector. In this chapter, the protective effects and mechanisms of melatonin on the cardiovascular system will be discussed.
Part of the book: Melatonin
Selenium (Se) is one of the trace elements that play an important role in many biological processes in the living body. Selenium acts in the body mainly in its forms called selenoprotein. Selenoproteins play a role in various events such as oxidative stress, immunity, cancer, inflammation, and endoplasmic reticulum stress. In selenium deficiency, the expression of selenoproteins and thus their activity decrease. In this case, some reactions such as increased oxidative stress, weakened immunity, endoplasmic reticulum stress, and inflammation cannot be prevented. The main source of selenium is food, and a diet poor in selenium causes selenium and therefore selenoprotein deficiency. This chapter will present information about the synthesis of selenoproteins and their role, especially in inflammation and endoplasmic reticulum stress response.
Part of the book: Selenium and Human Health
The endoplasmic reticulum (ER) is an organelle responsible for protein production in the cell and provides hemostasis in the cell. ER stress is stimulated by folded proteins, while the unfolded protein response (UPR) creates a response to ER stress and provides the cell survival. UPR modulation in mammals is provided with three major ER stress sensors, including transmembrane kinase 1, protein kinase-like ER kinase, and activating transcription factor 6. Because neurons are susceptible to misfolded proteins, severe or prolonged ER stress activates apoptotic cell death signals in the cell. Neurodegenerative diseases characterized by this condition are Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease, characterized by the accumulation and aggregation of misfolded proteins. In addition, ER stress can lead to depression, schizophrenia, sleep disruption, and post-traumatic stress disorders. Neurons are highly susceptible to protein misfolding and apoptotic cell death. For this reason, UPR modulation contributes to preventing the neurodegenerative process in cells with misfolded protein folding. The relationship between ER stress, UPR, and neuropathology is significant for understanding this process. This section will discuss the effects of ER stress between UPR modulation and neurodegenerative disorders, and the histopathological changes in the mentioned neurodegenerative diseases will be mentioned.
Part of the book: Molecular Histopathology and Cytopathology