Forensic Research & Technology

Biography

Biography: Alper Gumus

Abstract

Post mortem chemistry can provide quantitative results for determining post mortem interval (PMI). As a result of losing the function of the vital center in the brain stem cessation of respiration and circulation, known as somatic death. The development of this anoxic condition causes the death of cell and is called molecular cell death. The sudden interruption of ATP turnover leads to shock on the energy dependent mechanisms. One of the first affected organelle is cell membrane, the detoriation of active transport results in Na influx and K efflux because of loose of membrane permeability and leads to failure of membrane ion gradient. The catastrophic entrance of Ca in cytosol from organelles and cell exterior activates the phoslipases and causes to membrane rupture. With the loose of membrane integrity, fluid and soluble substance shift between compartments occur. Based on this phenomenon, levels of variety of parameters evaluated for PMI determination. Glucose is one of the most commonly analyzed parameters since the beginning of the post mortem chemistry. It has been reported that post mortem serum glucose levels in portal vein inferior vena cava and right atrium tend to decrease in vitrous humour. Degradation of liver glycogen molecules into free glucose with the subsequent diffusion of glycose to adjacent vessels has been reported as the cause of increment in the glucose levels. According to classical biochemistry knowledge, glycogenolysis is well organized metabolic process which is ATP dependent and advancing with the conjugate reactions. We planned an animal model study to determine why glucose levels increase in some tissues and decrease in others and we tried to determine the source of glucose in the tissues that exhibit increasing glucose after death. At the end of our study, we observed that post mortem glucose levels decreased in hepatic and muscle tissues and increased in renal and brain tissues. We observed that glycogen levels did not change in tissues by time. We were unable to confirm glycogen degradation. The cause of the glucose increase in vessels and organs adjacent to the liver is the diffusion of free glucose that is in the hepatic tissue during the antemortem period. We tried to estimate PMI using our findings. We created an ROC curve and the exact times of death of the subjects were used as the gold standart. The area under curve was 0.95, the slope of changes per unit time was highest for hepatic glucose levels. We determined cut-off levels with optimal sensitivity and specificity. Based on these calculations if a hepatic glucose levels is above the 279 mg/gprot death occurred with in 24 h with 90 % sensitivity and 92% specificity. If a glucose level is fewer than 163 mg/gprot death occurred more than 36 h. According to our studies, it is possible that an estimation of the PMI can be made using a biochemical marker. Our results are valid for selected environmental conditions. To accumulate sufficient data regarding this subject, additional studies should be performed using alternative tissues, parameters, and variable environmental conditions.