Mitochondria Case

Mitochondria are important because they allow our bodies to function by converting oxygen that we breathe in and the nutrients we ingest from food to energy we can use in the form of ATP (Adenosine triphosphate). This is done through aerobic respiration (requires oxygen), without the many mitochondria we have in our body we would not have sufficient energy from anaerobic respiration for our metabolic requirements. (Link its importance to its other functions- what would happen if it could not perform its functions e.g. lack of regulation of apoptosis and cancer- links to essays overall argument).

What it is: Mitochondria are a part of eukaryotic cells and it takes in nutrients from the body and breaks it down and then it eventually turns it into energy.

Until recent years, the mitochondrial genome, located in the mitochondrion, and the genetic information encoded by it have been given little attention. However, recently it became apparent that the mitochondrial genome, despite its small size, is crucial for the study of human evolution and disease, as mtDNA mutations lead to some serious diseases.

Mitochondria, dubbed the ‘powerhouse of the cell’, are a type of organelle present in most human cells. Their primary function is to generate Adenosine Triphosphate (ATP), the cell’s principal source of chemical energy. Unlike most other organelles, mitochondria store their own set of genetic material, distinct from the DNA situated in a cell’s nucleus. Although this ‘mitochondrial genome’ represents only 0.1% of a cell’s genetic information, it often plays a significant role in development.

Mitochondria are rod-shaped organelles that can be considered the power generators of a cell. They convert oxygen and nutrients into ATP. In turn, ATP powers most of the cell’s chemical reactions that allow the cell to function. Without mitochondria, certain cells would not be able to work and do their job. The cells would not be able to obtain enough energy to survive. A cell’s mitochondria relates to workers because they supply the cell with energy, just like how workers supply their energy to do their job. The mitochondria in a cell are responsible for providing energy so the cell can function, like how workers do certain tasks to keep the business thriving. Mitochondria are found in both plant and animal cells. However, they are found in

The shape of the mitochondria perfectly allows it to produce at their best. They are made of two membranes. The membrane on the inside folds over many times and creates cristae, a layered structure. The membrane on the outside acts like skin, and covers the organelle. Inside the mitochondria, there is a contained liquid called matrix. In the matrix we can find ribosomes and floating DNA. We can also find here granules, which are structures which may control concentrations of ions. The surface area inside the organelle increases due to the folding of the inner membrane. Many of the chemical reactions that occur in the mitochondria take place in the inner membrane, so this increased surface area gives more space for the chemical reactions to occur. It´s like this, you can get more work done if you have more space to do the work. We can observe similar strategies involving surface area in the microvilli in our intestines.

The hub of energy metabolism, the mitochondrion, is found in virtually all eukaryotic cells, with the exception being erythrocytes. The mitochondrion generates cellular energy in the form of adenosine triphosphate (ATP), mostly by means of the oxidative phosphorylation (OXPHOS) system that is located in the inner mitochondrial membrane. The respiratory chain (CI-CIV) and ATP synthase (CV) is collectively known as the OXPHOS system, encoded by both nuclear DNA (nDNA) and mitochondrial DNA (mtDNA). The number of mitochondria per cell, ranging from hundreds to thousands, is controlled by the energy requirements of specific tissues with the greatest abundance of mitochondria found in metabolic active tissue (Pieczenik and Neustadt, 2007). Mitochondrial disease is caused when there is a defect in any of the numerous mitochondrial pathways, due to spontaneous or inherited mutations. Respiratory chain deficiencies (RCDs) are the largest subgroup of mitochondrial disease and occur when one of the four respiratory chain complexes become impaired. RCDs are considered to be one of the most common

Presbycusis or Age-related hearing impairment is the most frequent sensory disorder in the adults. It affects more than half of all adults by age seventy-five years. Presbycusis is an irreversible symmetrical progressive loss of hearing sensitivity during the lifespan. It has an insidious onset without clinical manifestation so detected by the routine diagnostic test after losing or damaging to inner ear cells and neurons. Presbycusis counted as an untreatable disorder since these inner ear structures lose the ability of regeneration. Mitochondria by production reactive oxygen species or inducing apoptotic genes is one of most prominent intracellular organelles that contribute in presbycusis progression. The present study focused on mitochondrial

The article Replacing the cell’s power plants by Eric A. Shoubridge discusses the DNA found within mitochondria. Mitochondrial DNA (mtDNA) differs from nuclear DNA as it is inherited from only the mother. However, the mtDNA can also contain mutations which, similar to the nuclear DNA, have the potential to cause severe complications. Due to the mtDNA being restricted to the mitochondria multiple approaches have been developed in effort to reduce or prevent the amount and effect of mtDNA mutations.

This results in increased energy expenditure, fuel mobilization and oxidation for energy extraction, oxygen consumption, respiratory rate, and heat production and release (Dauncey.,1990). The stimulation of the respiratory rate would intuitively lead to greater ROS production but, the relation between these two variables is not linear. Instead, ROS production depends largely on the mitochondria. Mitochondria are the primary intracellular site of oxygen consumption and the major source of reactive oxygen species (ROS), most of them originating from the mitochondrial respiratory chain(Armstong &Jones.,2002). Although THs do not directly determine the respiratory state of the mitochondria (Katyare and Raian.,2005), stimulation by THs by augmenting ATP breakdown by different energy-consuming mechanisms in the cell (Dauncey.,1990) and thus increasing ADP availability. This would be expected to decrease ROS production. However, THs also promote a reduction state in the cell by increasing fuel availability and extramitochondrial production of ATP and NADH, which in turn promote reduction of the components of the mitochondrial respiratory chain

(8). Our preliminary data indicate that alveolar type (ATII) cells isolated from individuals with emphysema have higher nuclear DSBs than control smokers or nonsmokers. Moreover, we observed an increase in mtDNA damage in ATII cells in this disease in comparison with controls. We also found lower XRCC4-like factor (XLF) expression, which is involved in NHEJ pathway (9, 10), in ATII cells in emphysema in comparison with controls. Furthermore, we detected that high oxidative stress induced by exposure to cigarette smoke induces XLF oxidation and localization in mitochondria. DJ-1 is a cytoprotective protein localized in mitochondria. However, we observed that it interacts with XLF in ATII cells in emphysema, which indicates the critical role of XLF/DJ-1 complex in mitochondrial function. In addition, our results suggest that the number of mitochondria is decreased in these cells isolated from emphysema patients in comparison with control smokers and nonsmokers. Our hypothesis is that high levels of ROS in emphysema induce XLF oxidation and mtDNA damage leading to mitophagy and cell death (Fig. 1). Elucidating the molecular mechanisms contributing to mitophagy in primary ATII cells will advance our understanding of the contribution of mitochondria physiology to emphysema development. ATII cells will be isolated from excess tissue obtained from lung transplants of patients with emphysema, Veterans with respiratory problems and from control organ donors

Under normal conditions, the mitochondria maintain cytosolic Ca2+ levels, which is necessary for normal cellular function. However, the mitochondrial uptake of excessive levels of Ca2+ can lead to inhibition of ATP synthesis, disruption of mitochondrial membrane potential, increased ROS production, and generation of the mitochondrial permeability transition (mPT) state, which is thought to occur in response to formation of the mPT pore. As a consequence, cellular demise can occur through necrotic-related mechanisms events, including a loss of energy production and oxidative stress as well as apoptotic-related mechanisms, including the mitochondrial release of pro-apoptotic proteins. Given the central role of the mitochondria in cell

Reduced health problems or occurrence of disability causing diseases is one of the major problems in ageing process besides an extended life span. Daf-2 was one of the first few genes that were discovered to be directly involved in extending the lifespan of Caenorhabditis elegans (Kenyon et al., 1993). Considerable evidence in past has been provided by the association of mitochondrial abnormalities (Trifunovic and Larsson, 2008), genetic instability, altered intercellular signaling, an imbalance in hormones and reduced cell replacement capacity as key players in regulating cellular ageing (Figure 2 A). Being a central component involved in cellular metabolism and a major factor in disease occurrence, various studies utilizing protein quality

Mitochondria are often referred to as the powerhouses of the cells. They generate the energy that our cells need to do their jobs. For example, brain cells need a lot of energy to be able to communicate with each other and also to communicate with parts of the body that may be far away, to do this substances need to be transported along the cells, which needs lots of energy. Muscle fibres also need a lot of energy to help us to move, maintain our posture and lift objects.

Once a upon time, there was a lonely mitochondria named Sophia Mitochondria. Sophia Mitochondria had been alone for a while and she does not know where her parents are. She want to find her parents so she decided to talk someone to help her which is her childhood best friend, David Chloroplast. However, before she called him, she did her normal routine. She took nutrients from one of their cells, breaks it down and turn it into energy. This routine is also known as cellular respiration. After that, she call her David Chloroplast and thirty minutes later, David Chloroplast was in front of her house. David Chloroplast and Sophia Mitochondria came to Bacteria Garden which Sophia Mitochondria’s parents favorite place to go every weekend. When they