Necrosis Case Study

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components into surrounding tissue (121). Key players that help mediate necrosis include ROS, Calcium ions, poly-ADP-ribose-polymerase (PARP), and lysosomal proteases (888). PARP is an enzyme that is responsible for repairing DNA damage, such as strand breaks. Cells that have undergone a traumatic cellular insult typically have damaged DNA. PARP will deplete cellular ATP in an attempt to repair the massive damage to DNA. Several proteases are activated by increased cellular calcium ion concentration that degraded important cellular proteins. (888)
Necrosis is not nearly as regulated as apoptosis but there are a few steps that indicate necrosis is a programmed mechanism. The permanent opening of the MPTP by increased calcium concentration …show more content…
There are several mechanism in which lead (Pb 2+) leads to an increase in free radicals and decrease in antioxidant enzymes. Lead can bind and inhibit the antioxidant enzymes superoxide dismutase (SOD), catalase, glutathione (GSH) peroxidase and glutathione reductase. The inhibition capability of lead is manifested in the capacity of lead to bind thiol groups of protein and non-protein biomolecules. By binding thiol groups of the antioxidant enzymes, lead can inhibit the activity of the enzymes. Lead increases the amount of cellular ROS through mechanisms involving PKC and ALAD (878). Nicotinamide adenine dinucleotide phosphate (NADPH) complex produces reactive oxygen species (ROS) when the complex is reduced. PKC activated by lead can reduce NADPH complex, leading to release of ROS. ALAD produces δ-aminolevulinic acid when ALAD is inhibited. Buildup of δ-aminolevulinic acid poses a threat because δ-aminolevulinic acid can be oxidized to release ROS. Lead has the capability forming lead-superoxide complexes that allow the complex to have great oxidizing potential. Lead can elicit membrane damage to cells through lipid oxidation. Negatively charged phospholipids can be targeted by lead to carry out lipid oxidation

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