Gallbladder Case Study

Another type of injury to the gallbladder is caused by lipid peroxidation. Lipid peroxidation is a process that is naturally occurring in the body in minuscule amounts, mainly by many oxygen species effects, such as hydroxyl radicals and hydrogen peroxide. These species readily assault the polyunsaturated fatty acids in the membrane, which induces a self-propagating chain reaction. The destruction of the membrane lipids are hazardous for the sustainability of cells (Mylonas, 1999). This was seen in the gallbladders in broiler chickens when their food was laced with either 400 mg/kg or 600 mg/kg when compared to the control. Both of the experimental groups showed a significantly higher amount of sludge and a lower amount of volume in the gallbladder
than the control. When histological sections were collected, not only was it determined that the 400 mg/kg caused lymphocyte infiltration but it also caused severe periportal inflammatory reaction in the chickens given 600 mg/kg (Sipos, 2003) Injury to the gallbladder was believed to not only be caused by lipid peroxidation, but also a reduction in nitrogen oxide protection and an increase in the formation of hydroxyl radicals. Not only are these affects believed to increase the chance of creating gall stones, they are also believed decrease the size of the gallbladder and increase the thickness of its walls but effecting the cells proliferation and rise the tone of the gallbladder (Sipos, 2003) The next area that lead has an effect on in the gastrointestinal tract is the intestinal microflora.
The lead that is unabsorbed into the body has a direct influence on the guts biome and also its physiology. The gut flora has been described as a hidden organ that plays a crucial part in maintaining health. This makes maintaining hemostasis inside and out of the gastrointestinal tract vitally important. The epithelium of the gastrointestinal tract is of great importance because it provides a physical barrier, it decontaminates or eliminates detrimental intestinal substances, and it ensures the mucosal immune response. If there is any disturbance of the flora then, there is an amplified danger of resulting metabolic disorders, inflammatory, and allergic diseases (Breton,
2013). Lead effecting the gut flora was demonstrated in Balb/C female mice. They were exposed to either 100 ppm or 500 ppm of lead in their drinking water for eight weeks. The fecal pellets and cecal content were collected and analyzed along with the nucleic acid extraction. When analyzed by denaturing gradient gel electrophoresis (DGGE), it was determined that the murine microbiota was not significantly modified. A more comprehensive test was done on the fecal and cecal biome by a 454 pyrosequencing of the 16S rRNA, precisely the V5-V6 section. It was determined that two major phyla were copious, the Firmicutes and the Bacteroidetes, in all of the groups of mice. However, the Actinobacteria had a decrease in amount. It was also determined that there was a small but statistically significant difference in the Prevotellaceae and the Clostridiaceae, which breakdown proteins glucose respectively (Breton, 2013). There were substantial variances in a number of the other families of bacterial flora in the biome in both the fecal and cecal samples. There was a low number of Lachnospiraceae and a high number of Lactobacillaceae. A low number of Lachnospiraceae and a low diversity of bacteria have been linked as a susceptibility to colitis. The Lactobacillaceae is a lactic acid bacteria and an increase in this bacteria will increase the lactic acid in the gut. The low or high number of certain bacteria flora have been linked to intestinal inflammation. This is due to either an impact on the intestinal homeostasis or the alimentary tract. The last exocrine gland that lead effects is the pancreas.
It was determined that 71% of labeled lead Pb210 was linked with mitochondrial sub fraction of the pancrea. It was observed that the lead was deposited in both the matrix and the inner membrane of the mitochondria. Lead bound to the mitochondria was predominantly stable. The next study was done to evaluate the effect of lead on the acinar cells of the mitochondria, which produces digestive enzymes, and the ultrastructure. It was carried out on 45 male Wistar rats that were given either 50 mg/dm3 or 500 mg/dm3 if they were not in the control group (Szynaka,
1999). It was determined that the cytochrome oxidase in the pancreas after lead was introduced to the rats decreased, as seen in Table 2. The activity of the cytochrome oxidase decreased by 15% and 37% in both 50 mg/dm3 and 500 mg/dm3 respectively after the first two weeks. After six weeks, the activity decreased to 55% for the 50 mg/dm3 and 70% for the 500 mg/dm3 when compared to the control group. Two weeks after the treatment of lead stopped, the activity increased in both groups.