Factors Of Postnatal Hyperoxia And Premature Aging

Because the PCO2 levels are too high the body is not getting the adequate amount of oxygen. This means the oxygen-carrying hemoglobin is not working properly do to the excessive amounts carbon dioxide causing respiratory acidosis.

The length of the telomere indicates age-related diseases, unhealthy lifestyle, and longevity in the lifespan.

One of the many changes that affect us every day is oxygen toxicity in premature

This causes further damage to the lung. This hyperinflation of the lung is known as emphysema. In emphysema, the alveoli are permanently enlarged leading to a dramatic decline in the alveolar surface area available for gas exchange (Workman, 2013). The permanent enlargement of the alveoli is caused by the overabundance of proteases. When proteases are present in higher-than-normal levels, alveoli is damaged as the proteases break down the elastin located within the lung. When elastin is broken down, lung elasticity is decreased and air is permanently trapped within the air spaces (Workman, 2013). These overall changes from both bronchitis and emphysema lead to hypoxemia, decreased oxygenation, and respiratory

Chronic hypoxic events during pregnancy associated with mild to moderate maternal hypertension have shown however to sometime accelerate fetal lung maturity and surfactant production leading to a decrease in neonatal respiratory complications. (Kim, Vohr, & Oh, 39) This due to cortical steroid secretion that stimulate an increased production of surfactant in response to the stresses of hypoxic events. (Porth, 1306)

These cellular defects eventually interfere with the normal function of the cells causing disabilities and disease (Kirkwood, 2008). Senescence results in an increased mortality rate and a decrease in the ability to produce offspring. A person’s average lifespan correlates with their senescence rate (Bergstrom, 2012). Genes are thought to account for one fourth of what determines the length of an individual’s lifetime will be. Genes also shape an individual's life history in relationship to their reproduction and survival. The genes that are believed to have a major effect on aging are those which are involved in the regulation of metabolism (Kirkwood, 2008).

A recent study investigated the effect of H2S deficiency on endothelial NO synthase (eNOS) function, NO production, and ischemia / reperfusion injury by on CSE- knocked out mice and control [12]. Significant Lower H2S levels among CSE- knocked out mice was confirmed by gas chromatography. From oxidative stress perspective; their results revealed significant higher levels of malondialdehyde (indicator for lipid peroxidation) in heart muscle among CSE- knocked out mice compared to

Mitochondrial play a crucial role in energy transduction of myocardium. Cellular and mitochondria metabolism observed in the course of hyperglycemia is associated with excessive production of reactive oxygen species (ROS). Among other factors involve in ROS production, is intracellular concentration of glucose secreted by the pancreatic β cells. Glucose play a key role in the mitochondrial-dependent oxidative reaction thus involvement of insulin resistance contribute to the influx of calcium ion Ca2+, generating excessive ROS. Therefore, mitochondrial radical ROS production in response to hyperglycemia is associated with Ca2+ concentration linked to cardiac mitochondrial dysfunction.

MAO is the enzyme responsible for degradation of endogenous monoamine neurotransmitters and dietary amines, e.g. tyramine. Recently the cardiovascular field has focused on the role of MAO activity in the heart demonstrating the role of MAO-A as an important myocardial source of reactive oxygen species(ROS).(5) Depending on the concentrations of the available substrate, ROS produced by MAO-A are able to trigger separate signaling pathways leading respectively to cell proliferation and hypertrophy or apoptosis .

Telomeres are the repeating end caps of chromosomes. As a cell divides and duplicates, the telomere genes began to shorten. The shortening of the genetic end caps is considered a biological clock which counts down to a cellular death, also known as apoptosis. Aging is accompanied by telomere shortening and it has been discovered in age related diseases, such as premature aging syndromes. The consequences of a telomere dysfunction are very diverse and can include nail dystrophy, abnormalities in skin pigmentation, aplastic anemia, pulmonary fibrosis, and a rapidly expanding list of other diseases. The erosion of the telomere genes is meant to suppress malignant transformations. In exceptional cases, it can cause chromosomal instability and promote the formation of tumors. Telomerase is the enzyme which can replace telomere genes lost through cellular senescence. Unregulated expression of telomerase has been seen in a majority of cancers. Telomerase is a double edged sword as it allows cancerous cells to divide without regulation. The accumulated evidence on telomere genes would suggest that they have the ability to maintain telomere length and to mask them from recognition as damaged DNA. Understanding telomerase regulation and telomere length maintenance will uncover many mysteries in the control of aging and

“Pediatric respiratory failure develops when the rate of gas exchange between the atmosphere and the blood is unable to match the body's metabolic demands” (Springer, 2014).

Accumulation of DNA damage occurs with increasing age, causing cells to deteriorate and malfunction. While DNA damages incur constantly in cells of living organisms, most of the damages are repaired in healthy individuals. However, some DNA damage accumulate as the DNA polymerases and other repair mechanisms cannot correct defects at a rapid enough pace as the rate of damage. In particular, damage to mitochondrial DNA may lead to mitochondrial dysfunction. Maintenance of metabolic homeostasis along with appropriate stress responses absolutely requires proper mitochondrial function. Mitochondrial dysfunction is known to play a critical role in aging and as well as other numerous human diseases, for example cancer and neurodegenerative disorders

In particular: a) species which show no aging (“animals with negligible senescence”) show the same telomerase activity at any age and have no cancer problem, as demonstrated by their constant mortality rate at any age; b) in our species, studied in wild conditions, the increase in age-related mortality is precedent to cancer-related deaths cases and it is impossible that defenses against cancer kill before cancer can develop; c) shortened telomeres, as a result of telomerase inactivity, cause dysfunctional telomere-induced instability and so the likelihood of cancer increases; d) in normal mice, telomerase expression delays aging but does not increase cancer risk.

Predominantly human cancers emerge during ageing or during the end stage of disease are caused by the increased rate of chromosomal instability, thus inducing lesions responsible for apoptosis within cells altering them into immortal cells, i.e. cancer cells. Telomere shortening has very strong ties to the increased risk of immortal cells occurring within ageing and chronic disease, showing a very strong indication that the shortening of sequence affects cell division; this directly contributes to the chromosomal instability and cancer initiation processes.

The oxidative stress can cause cell damage, resulting in inflammation, which has also been found to be a major contributor to disease progression of GM2 gangliosidosis [17]. In this study, we identified elevation in glutathione pathways, which plays a pivotal role in responses to oxidative stress. Another evidence of inflammation is reduced levels of arachidonic acid, an omega-6 fatty acid, in brain samples of SD mice. Oxidation of arachidonic acid can generate leukotrienes, a family of eicosanoid inflammatory mediators produced in leukocytes, and thus promote inflammation. The increased energy requirements can also activate autophagy and protein catabolism, which have been found in MPS I and MPS VII mice [13]. In this study, we found increased levels of amino acids, amino acid derivatives and dipeptides, indicating increased protein catabolism. Increased requirements of energy and raw materials can also activate lipid metabolism and carbohydrate metabolism, manifested by decreased adiposity, a common observation in many lysosomal diseases [18-20]. In addition, the enlarged lysosome and distended cells due to abnormal accumulation requires increased membrane synthesis, which can also affect lipid metabolism. Our previous proteomic analysis [21] also identified abnormality in the cytoskeleton system, which can be partially attributed to altered cellular architecture due to storage accumulation. Collectively, we show here that the energy imbalance caused by the lack of