Oxidative stress

Oxidative stress is one of the most important stimuli that initiates CCl4 mediated liver damage. Lipid peroxidation as result of oxidative stress is well known to be involved in the liver injury (Lin et al., 2012). There are a number of studies that has reported the alkynated halogen CCl4 to be widely used as a hepatotoxin to induce liver toxicity in experimental animal models (Weber et al., 2003). Analysis of histopathology revealed that intragastric administration of CCl4 causes damage to the hepatic

Oxidative stress promotion: Disturbance of the prooxidant-antioxidant balance in favour of the former is termed as oxidative stress (Aly et al. 2010; Uchendu et al. 2012). The outcome of this multistep process is tissue damage which builds a path from the onset of tissue damage through diseases to finally apoptosis (Agrawal and Sharma 2010). Damage induced by oxidative stress occurs through the production of reactive oxygen species (ROS) which includes oxygen derived free radicals such as superoxide

Upon an oxidative stress, thioredoxin becomes oxidized and disassociates from ASK-1, leading to activation of JNK and p38 pathways through oligomerization of ASK-1 [20]. Several reports provide evidence that JNK activation as pro-apoptotic kinases in response to cerebral

signaling but an imbalance in favor of reactive oxygen species results in oxidative stress (OS) (Kashmiri et al.,2014). Oxidative stress (OS) result in interference in the functioning of biological systems that maintain levels of environmentally produced reactive oxygen species (ROS), by readily detecting and detoxifying them (Lucana et al., 2012). Living organisms have adopted mechanisms to protect themselves against oxidative stress, by producing enzymes such as catalase and superoxide dismutase, small

Module ten discussed oxidative stress, and the causes, as well as consequences of liver disorders. Oxidative stress occurs when there is an abnormal balance between nonspecific oxidation reactions, and the body's ability to counteract them. A nonspecific oxidation reaction refers to one that involves free radicals reacting in a disorderly fashion with other molecules. Free radicals are highly reactive molecules that can cause cellular damage, targeting that of carbohydrates, lipids, proteins and

sources of antioxidants should be a part of one's daily diet, in order to reduce oxidative stress and related

The study of oxidative stress and obesity has stimulated several attempts in recent times to define the contribution of the individual components of the metabolic syndrome to oxidative stress as it is in metabolic syndrome patients. Although there have been recent attempts to do so, studies have revealed the role of obesity as a critical and core component in the development of metabolic syndrome. Essentially, obesity plays an integral role in amplifying oxidative stress. It has been proven that

Oxidative stress response during infection Candida albicans inside phagocytes After internalization of C. albicans in phagocytes, it has been observed that the target fungal pathogen like any other microbial pathogen follows the path from phagosomes to phagolysosomes and gets fumigated and killed. During infection, Candida species are exposed to higher levels of reactive oxygen species (ROS), reactive nitrogen species (RNS) and antimicrobial peptides, low pH and reactive chloride species (HOCl) inside

(over 120/80 mm Hg) in order for quercetin supplementation to show effects. Also in Askari et al. (2012), they found that Vitamin C was needed for quercetin supplementation to decrease oxidative stress. When one exercises excessively there is an increase in oxygen consumption which can lead to oxidative stress

intrinsic and extrinsic pathway (Elmore, 2007). When MD patients engage in high-intensity exercises cause a decrease in the production of ROS that makes cells in the intrinsic pathway to self-engage and kill themselves as they are sensitive to the stress on the cells. The death that occurs in the cells in the extrinsic pathway is thought to be due to the activation of the caspases that cause the death of cells and enzymes that debase protein functions. In the case of extrinsic pathway cell death,