Cell injury and cell death Essay example

With all living organisms, a process known as cell respiration is integral in order to provide the body with an essential form of energy, adenosine triphosphate (ATP). Oxygen, although an essential part of this process, can form reactants from colliding with electrons associated with carrier molecules. (pb101.rcsb.org, 2017). Hydrogen peroxide is an integral product of this reaction but is known to impose negative effects on the body if high levels are introduced. Explicitly, this reaction is caused “If oxygen runs into (one of these) carrier molecules, the electron may be accidentally transferred to it. This converts oxygen into dangerous compounds such as superoxide radicals and hydrogen peroxide, which can attack the delicate sulphur atoms and metal ions in proteins.” (pdbh101.rcb.org, 2017). Research has suggested that the hydrogen peroxide can be converted into hydroxyl radicals, known to mutate DNA, which can potentially cause bodily harm due to DNA’s role in the synthesis of proteins. These radicals can cause detrimental effects on the human body, and studies have suggested a link to ageing. Due to the harmful effects of these H2o2, it is important that the body finds a way to dispose of hydrogen peroxide before concentrations are too great.

Everyone is susceptible to the dangers of lead contamination; but children are especially at risk. High levels of lead in children can lead to brain and kidney damage and damage to red blood cells. Low levels of lead can also cause problems that are less life-threatening but can be just as devastating, like low IQ, hearing and language impairment, reduced attention span and poor school performance. In adults, exposure to lead can lead to an increased risk for high blood pressure. Pregnant women and their fetuses are extremely vulnerable to lead. In women, lead increases the risk of infertility and miscarriages; in fetuses, lead can cause low birth weight, premature birth and impaired mental and physical development.

For example, cellular swelling occurs due to cellular hypoxia, which damages the sodium-potassium membrane pump; as well as fatty change it can impair cellular function and damage the cell ability of adequately metabolize fat. Both situations are reversible when the causes are eliminated. In contrast, irreversible cell injury is the cell death with continuing damage, the injury becomes irreversible, which the cell cannot recover and dies. There are two types of cell death necrosis and apoptosis. When damage to membranes is severe, enzymes leak out of lysosomes, enter the cytoplasm, and digest the cell, resulting in necrosis ( McCance & Huether, 2014). Necrosis is the major pathway of cell death in many commonly encountered injuries, for example resulting from ischemia, exposure to toxins, various infections, and

Many may not know Parkinson’s disease is the second most common neurodegenerative disorder in the world. This disease is most seen in the elderly starting at 62 years of age although, younger individuals can still have the disease it isn’t common. Parkinson’s make it difficult for its victims to carry out everyday activities that might have once been easy for them. As the disease progresses it makes it hard for the patient to do things like walk, stand, swallow and speak. A great deal of people don’t realize how helpful therapy can be when dealing with such disease!

When lead enters the human body, it is distributed to the brain, liver, kidney and bones. It is deposited in the teeth and bones where it accumulates over time. Exposure to high levels of lead may cause anemia, kidney and brain damage. Lead exposure can also cause miscarriage and infertility. The effects are even more severe in children. Lead can affect children’s brain development resulting in decreased intelligence quotient (IQ), shortened attention span and increased antisocial behaviour. At high levels of exposure, lead may attack the brain and central nervous system, causing coma. Children who survive severe lead poisoning may continue to suffer mental retardation and behavioural disorders. Furthermore, pregnant woman exposed to lead can

DNA is composed of two strands with molecules binding to either both strands or only one strand. If the cell attempts to reproduce crosslinked DNA while it is going through cell division the strand of DNA can break, leading to apoptosis, which is programmed cell death.4 The category of alkylating agents has many subcategories of chemicals. The nitrogen mustards include mechlorethamine, chlorambucil, cyclophosphamide, ifosfamide, and melphalan.5 The group nitrosoureas includes streptozicin, carmustine, and lomustine.5 Alkyl sulfates include one chemical called busulfan.5 The subcategory known as triazines includes dacarbazine and temozolomide. The ethylenimines include thiotepa and alretamine.5 Since these drugs inhibit cell replication, there is a lot of damage done to the human body. One very detrimental piece of damage that is done is long-term damage to bone marrow.5 Bone marrow is responsible for producing the blood cells in the body. It holds hematopoietic stem cells, which allow for the production of white blood cells, red blood cells, and platelets. White blood cells are what allow our bodies to fight off infection, so if there is damage to the bone marrow, our body will not produce white blood cells in an effective manner which will ultimately make us more susceptible to infection or disease. Red blood cells carry oxygen throughout the body as well

Lead exposure causes permanent brain damage. Children under six are most at risk from small amounts of lead. Among adults, pregnant women are especially at risk from exposure to lead. In children, lead can cause nervous system and kidney damage, decreased intelligence, attention deficit disorder, learning disabilities; speech, language, and behavior problems. In pregnant women, lead is passed from the mother to the fetus and can cause miscarriages, premature births, brain damage, and low birth weight.

These superoxides may be dangerous because they alter the structure of iron and protein via reduction. They may also undergo dismutation to form hydrogen peroxide which, in turn, gives rise to hydroxyl radicals, the most reactive ROS (Gulumian and Van Wyk, 1987; Agarwal et al., 2005). Hydrogen peroxide is not a free radical but its neutral charge allows it to pass through cell membranes and so this makes it very dangerous (Kurutas, 2015). Other internal or endogenous sources for these free radicals are inflammation, xanthine oxidase, peroxisomes, phagocytosis, exercise and ischaemia. Exogenous factors which lead to the development of these ROS include smoking, ozone, environmental pollutants, radiation, pesticides and drugs (Lobo et al.,

There are several cellular injury mechanisms that result in a variety of different diseases. One general mechanism of cellular injury is through chemical injury. There are about 4 billion pounds of toxic chemicals released per year in the United States, and of these, 72 million pounds are known carcinogens (Huether).

anemia. The process is called apheresis, which avoids overloading the patient’s body with iron, thus removing damaged cells from circulation. Although this has been

· Extreme pain is due to the hypoxic environment that results from the occlusion of capillary beds within tissues by sickled RBCs. This sickling is due to the polymerization of HbS in low-oxygen environments occluding tissues and causing local hypoxic environments. Inflammation is indicated as the trigger for this process in many cases. Experimental studies in transgenic HbS homozygote mice using hypoxia and inflammatory drugs showed occlusion of the postcapillary venules due to increased interactions between leukocytes, RBCs, and the vascular endothelium. In addition, precapillary obstruction is observed in sickled RBCs with especially high [HbS] and increased interactions between the vascular endothelium and RBCs. The tissue damage that results from the hypoxic environment leads to an increase in inflammation in the area once the tissue is repurfused with

An irritant, such as cigarette smoke, effects the cells of the epithelium lining. Initially the body can repair the cell, but with repeated exposure the cells of the lungs become damaged and grow uncontrollably. P53 is a gene for various downstream targets that are involved in cell progression, DNA repair and regulation of cells that undergo apoptosis. Mutations to P53 hinder its normal tumor suppressing capabilities. Therefore, DNA damage remains unchecked, faulty cells proceed through the cell cycle and apoptosis is invaded. All these factors create a genetic condition where the cell is more susceptible to further mutation. If the cancer grows large enough, it can affect the organ by closing off the aveoli, leading to shortness of

Although DNA remains mostly stable, it is constantly subject to chemical modification from a variety of different sources. Numerous forms of DNA damage have been identified resulting from different factors such as alkylating agents, hydrolytic deamination, free radicals, and mismatching base pairs. Alkylating agents cause mutations of legitimate bases, transforming them in to either a non-coding or lethal lesion in the DNA. Hydrolytic deamination changes on base on the DNA double helix into another. (Sinha & Häder, 2002) Oxygen radicals are generated during cellular production of O2 gas is known to either attack the bases of DNA (A, T C, or G) or the Deoxyribose to damage the DNA bases or break strands. (Marnett, 2000) DNA remains under threat by other cellular factors, but it does have certain mechanisms in place to repair certain

It can damage DNA, proteins and lipid membranes, and it may be a causing factor of cancer. If the hydrogen peroxide in our bodies is not broken down into water and oxygen, then the buildup of the hydrogen peroxide will kill humans. Since hydrogen peroxide is toxic to the body, the body has developed a way to get rid of the hydrogen peroxide in the body by producing an enzyme to act as

Critical events in ischemic cascade. Adapted from Midori et al. (2012) (17). Following ischaemia, the deprivation of oxygen and glucose to the brain lead to loss of ATP (energy loss) and ion pump failure. The loss of ion concentration gradients causing to cytotoxic oedema and releasing of excitatory amino acids (EAAs). Following glucose lessening cell aerobic metabolism switch to anaerobic, which resulting to metabolic acidosis. All of these events lead to cell death, or necrosis. Ischaemia also caused to the upregulation and activation of many immediate early genes and stress signals, which lead to inflammatory responses, cell apoptosis and, subsequently, activation of matrix metalloproteinases (MMPs) as a damaging protease which can lead