Oxidative stress is the increase in cellular oxidant concentration in comparison to antioxidant titer. Toxic insults and many other diseased conditions are mediated through the formation of such condition. Once the redox equilibrium is disrupted, the cellular antioxidant system functions to bring back the cell to redox homeostasis state. The field players of the cytoprotective machinery are the xenobiotic‐metabolizing enzymes that are transcriptionally controlled by upstream regulatory pathways like the Nrf2–ARE pathway and AhR–XRE pathway. The importance of Nrf2 lies in the fact that it is activated by a variety of compounds and has a wide range of inducers including metals, organic toxicants and so forth. The present review article aims to discuss the role of Nrf2 in cellular protection and also intends to illuminate the regulatory mechanisms that control Nrf2 itself. This can add to our knowledge of how the cell reacts and survives against such stressed conditions.

The eukaryotic initiation factor 2 (eIF-2)-associated 67-kDa polypeptide (p67) isolated from reticulocyte lysate protects the eIF-2 a subunit from eIF-2 kinase-catalyzed phosphorylation and promotes protein synthesis in the presence of active eIF-2 kinases. is a critical factor in protein synthesis regulation in animal cells.

Selective low (15 mg sodium fluoride (NaF)/L) and relatively high (150 mg NaF/L) doses of in vivo fluoride (F) treatment to Swiss albino mice through drinking water elicited organ-specific toxicological response. All the F-exposed groups showed severe alterations in both liver and kidney architectures, but there was no significant change in the rate of water consumption and body weight. Vacuolar degeneration, micronecrotic foci in the hepatocytes, and hepatocellular hypertrophy were evident in the mice exposed to low dose (15 mg NaF/L for 30 days) while sinusoidal dilation with enlarged central vein surrounded by deep-blue erythrocytes were preponderant when treated with the same dose for a period of 90 days. Blood filled spaces, disintegration of tubular epithelium, and atrophy of glomeruli were also recorded in the kidney of the same treatment group. Change in reduced glutathione level (GSH), glutathione-s-transferase (GST) activity, malondialdehyde (MDA) production in both liver and kidney, disturbances in liver function, induction of heat shock protein 70 (Hsp 70) expression in kidney and its down regulation in liver were positively correlated with histopathological lesion.

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Since the work of Watson and Crick in the mid-1950s, the science of genetics has become increasingly molecular. The development of recombinant DNA technologies by the agricultural and pharmaceutical industries led to the introduction of genetically modified organisms (GMOs). By the end of the twentieth century, reports of animal cloning and recent completion of the Human Genome Project (HGP), as well techniques developed for DNA fingerprinting, gene therapy and others, raised important ethical and social issues about the applications of such technologies. For citizens to understand these issues, appropriate genetics education is needed in schools. A good foundation in genetics also requires knowledge and understanding of topics such as structure and function of cells, cell division, and reproduction. Studies at the international level report poor understanding by students of genetics and genetic technologies, with widespread misconceptions at various levels. Similar studies were nearly absent in India. In this study, I examine Indian higher secondary students' understanding of genetic information related to cells and transmission of genetic information during reproduction. Although preliminary in nature, the results provide cause for concern over the status of genetics education in India. The nature of students' conceptual understandings and possible reasons for the observed lack of understanding are discussed