Mechanism Behind Cystine-Tellurite Blood Agar free essay sample

These tellurite-resistant bacteria reduce tellurite to its elemental less toxic form tellurium Te0 intracellularly. The result is the accumulation of black deposits inside the cell is due to either internal or periplasmic accumulation of Te. Tellurite toxicity results from its ability to act as a strong oxidizing agent over a variety of cell components. Tellurite could exert its toxicity through intracellular generation of reactive oxygen species (ROS). Tellurite inhibits the cellular response to oxidative stresses. To inhibit the growth of most normal bacterial inhabitants of the upper respiratory tract, including most species of Streptococcus and Staphylococcus, is to inhibit the growth of aerobic organisms through the presence of oxygen and high concentration of tellurite. Reactive oxygen species compounds such as hydrogen peroxide (H2O2), superoxide anion (O2-) and hydroxyl redical (OH-) are natural byproducts of the normal metabolism of oxygen that can be formed by exposure of cells to free-radical generating molecules like metals and metalloids. We will write a custom essay sample on Mechanism Behind Cystine-Tellurite Blood Agar or any similar topic specifically for you Do Not WasteYour Time HIRE WRITER Only 13.90 / page ROS compounds are generally very small molecules and are highly reactive due to the presence of unpaired valence shell electrons. Increase of ROS levels dramatically due to the action of tellurite will result in significant damage to cell structures. This situation is known as oxidative stress. Generally, harmful effects of reactive oxygen species on the cell are most often: 1. damage of DNA 2. oxidations of polydesaturated fatty acids in lipids 3. xidations of amino acids in proteins 4. oxidatively inactivate specific enzymes by oxidation of co-factors In aerobic organisms, the energy needed to fuel biological functions is produced in the mitochondria via the electron transport chain, in addition to energy reactive oxygen species (ROS) are produced which have the potential to cause cellular damage. ROS can damage DNA, RNA, and proteins. Hydrogen peroxide (H2O2) is converted from superoxide that leaks from the mitochondria. Within the bacterial cell, there is catalase and superoxide dismutase that help to minimize the damaging effects of hydrogen peroxide by converting it into oxygen and water, benign molecules, however this conversion is not 100% efficient, and residual peroxides persist in the cell. Thus, excessive amounts of can cause damage to the bacterial cell. The resistance of C. diphtheriae to tellurite increases approximately ten-fold when cells are grown under anaerobic conditions, which is presumably due to the cell’s inability to produce ROS products under oxygen deprivation conditions. Gram-positive bacteria have an intrinsic low-level resistance to TeO32? , while high-level resistance has been determined in certain gram-negative obligate aerobic photosynthetic species. The capacity of these bacteria to grow at the presence of high tellurite concentrations depends on two factors: a. Plasmids (such as IncHI, IncHII, and IncP plasmids) have genetic determinants that allows the adaption of tellurite-resistant organisms to survive. b. Chromosomal genes important for growth in the presence of K2TeO3 have been identified in a few species, but their role has not been clearly determined. Most gram-negative bacteria do not grow in the presence of tellurite because they do not have these plasmids and chromosomal genes to help in the adaption. Most tellurite toxicity takes place in an aerobic environment. The increasing level of resistance of an organism depends primarily on the absence of oxygen. References: