Examining Compounds That Affect Mitochondrial Transport Essay

Succinate dehydrogenase is an enzyme found in the mitochondrial inner membrane. The enzyme catalyzes the reaction of oxidizing its substrate, succinate, into fumarate via the removal of hydrogen ions from succinate. This oxidation is vital in the Krebs cycle.

b) Janine made this statement: “… if your brain doesn’t get carbs—well, glucose, anyway—you get

gluconeogenesis slow down in which release of glucose to the blood stream is also slowed down

In the United Kingdom alone, 150 new born children per year suffer from life threatening, mitochondrial diseases. These diseases vary in severity from person to person, making them difficult to diagnose, and they inflict an array of ailments such as neurological problems, muscle weakness, visual or auditory impairments, heart, liver, and kidney disease,

In this class, we focused on Alzheimer's, specifically how it affected the person. I found myself especially drawn to the chemistry behind it and how the brain was altered in ways that couldn't be examined until the autopsy. Alzheimer’s is a disease that as of yet has no cure, but has the potential to affect a fair majority of the population in the future. In view of this, I want to approach potential treatments neurological diseases such as Alzheimer's and Parkinson’s from a chemical standpoint and attempt to find preventative measures if not a cure. With this in mind, my interests lie in both organic chemistry and biochemistry. I am interested in the use of organic synthesis to create new medically useful compounds. Moreover, I am interested in the neurological responses and biological effects of the newly created compounds and how said compounds are applicable in the medical

Mitochondrial dysfunction and oxidative stress have been consistently observed in brains of PD patients. There is increasing pharmacological and genetic evidence sustain a link between PD and mitochondrial respiratory chain dysfunction, particular a deficit in mitochondrial complex I (Franco-Iborra et al., 2015). Accidental exposure to 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine (MPTP), an mitochondrial complex I inhibitor, has been known to result in acute and irreversible syndrome that was almost indistinguishable from PD (Calne and Langston, 1983; Langston and Ballard, 1983). Later on, mitochondrial complex I inhibition has been identified in the brains of sporadic PD patients (Schapira et al., 1990). In addition, chronic systemic inhibition of mitochondrial complex I by pesticide rotenone has been found to link to sporadic PD (Betarbet et al., 2000). Interestingly, mitochondrial complex I deficiency has been found not only in the postmortem substantia nigra but also in cerebral cortex (Schapira et al., 1990), which is consistent to the cortical glucose hypometabolism observed in PD patients. Indeed, the pathology of PD has been found to involve several brain regions other than the SNc and many neurotransmitters other than dopamine (Lang and Obeso, 2004a, b). PD models using MPTP and rotenone have now been used extensively in PD research (Beal,

The discovery from the Scripps Research Institute in Florida shows promising results in tackling down the cause of Parkinson’s, and their outcomes led to a funding by the National Institutional Disorders and Stroke Research (NINDS). Research staff within the campus discovers that many diseases that relate in twisting a protein from its original structure will result in a cellular death but it isn’t due to the deformed shape. According to the article “Scripps Florida Scientists' 'Mad Cow' Discovery” (2015), one primal cause that leads to Parkinson’s is the lack of “NAD+” which later prohibits the proper energy function of the mitochondria. Researchers further delved into the study to find out this is preventable, by providing the misshaped protein

In this paper I will explain how metabolism works and the thyroid gland function in the human body. First the two different types of metabolism: Anabolism, Catabolism and how the nutrition also affects the production of the thyroid hormone. Secondly, the function of the thyroid hormone, which organs regulate, consequences if the human body begins if it works to work to fast or too slow. Third, the different hormones that the thyroid gland produces and how it regulates the metabolism. Fourth, there is certain nutrients that help the thyroid gland to produce the hormone and also there is another ones that affect the production of the thyroid hormone. Last how the six different types of thyroid problems are found, the symptoms and how they

Explain the role of RNA polymerase inhibition in causing the poisonous effect of the death cap mushroom.

Lundkvist, J., Halldin, M., Sandin, J., Nordvall, G., Forsell, P., Svensson, S., ... Ekstrand, J. (2014). The battle of Alzheimer's disease - the beginning of the future Unleashing the potential of academic discoveries. Frontiers in Pharmacology,

Mitochondrial damage is therefore a serious threat to the viability of the acinar and ductal cells, as well as the pancreas as a whole. Bile acids and ethanol metabolites, among the most common pancreatitis-inducing factors, act by causing the release of stored Ca2+ within the ER and inducing extracellular Ca2+ influx. This prolonged increase in cytosolic Ca2+ concentration leads to mitochondrial Ca2+ overload and decreased intracellular ATP levels. SERCA and PMCA pumps, which remove Ca2+ from the cytoplasm, require ATP to function and will become less active; further contributing to the sustained elevation of cytosolic Ca2+ concentration. This continuous overload causes mitochondrial membrane permeabilization and overall damage to the mitochondria.

The news story that I continue to research, Healthy mitochondria could stop Alzheimer’s, is directly related to finding the cause and cure for Alzheimer’s disease. Today’s research and treatment attempts for Alzheimer’s disease center around the belief that the cause of this disease is the build-up of toxic plaque in the brain due to the protein called beta-amyloid. This article introduces the thought that Alzheimer’s may be a metabolic disease and studies mitochondria, energy-producing cells. Specifically, scientists introduced the idea that healthy mitochondria can stop Alzheimer’s disease. Furthermore, studies reveal that Alzheimer’s disease causes damage to mitochondria resulting in the cell’s inability to protect or discard damaged cells.

(I) Regulation of mitochondrial transport during synapse formation and long-term depression (LTD). We have made now developed a highly robust assay for quantifying kinesin mediated transport in Aplysia sensory neurons (SNs). Our assay consists of time-lapse imaging of fluorescently labeled mitochondria in sensory neurons. We used mitotracker green to visualize

A newer model for toxin-induced Parkinsonism is based on the herbizide rotenone. Rotenone is the most potent member of the rotenoids, a family of natural cytotoxic compounds extracted from various parts of Leguminosa plants. Like MPTP, rotenone is highly lipophilic and brain distribution is heterogeneous paralleling regional differences in oxidative metabolism (Talpade, Greene et al. 2000). In mitochondria, rotenone impairs oxidative phosphorylation by inhibiting nicotinamide adenine dinucleotide (NADH)-ubiquinone reductase activity through its binding to the PSST subunit of the multipolypeptide enzyme complex I of the electron transport chain (Schuler and Casida 2001). Aside from its action on mitochondrial respiration, rotenone also inhibits

& Zeillin, R. (2012). Cotinine A potential new therapeutic agent against Alzheimer's disease. CNS Neuroscience & therapeutics. 18(7), 517-523