Perinatal Asphyxia Research Paper

In the present study, the MDA level was measured as an index of lipid peroxidation in order to observe the effect of caffeine on the oxidative stress induced by AlCl3 in cortex, hippocampus and striatum brain areas. Brain tissues are more vulnerable to oxidative stress other than tissues for many reasons such as high oxygen consumption (more than 20% of the total inspired oxygen), the presence of abundant amount of polyunsaturated fatty acids which are susceptible to free radicals attack, low antioxidant levels, high iron content in addition to the non-regenerative nature of neurons (Nehru and Anand, 2005; Kim et al., 2015). All these reasons may explain why brain is more susceptible to aluminum toxicity than other organs. In the present

of anesthetics by 50%, provides neuroprotection against focal cerebral ischemia. Perinatal asphyxia can lead to death and severe disability. Brain hypoxia-ischemia (HI) injury is the major pathophysiology contributing to death and severe disability after perinatal asphyxia. Ren et al. studied the effects of dexmedetomidine on seven-day old Sprague Dawley rats with

Although not labeled for use in patients under the age of 18 years, recently it has been introduced into the NICU setting for procedural use, as well as short-term sedation. There are no structured reviews on the efficacy and safety profile of dexmedetomidine; however, animal studies have documented its potential neuroprotective effects and minimal respiratory side effects. A study out of Berlin examined the neuroprotective features of dexmedetomidine in reducing the detrimental effects of oxygen toxicity. Following single doses of dexmedetomidine at various concentrations, six-day old rats in the treatment group were exposed to 80% fiO2 for 24 hrs. Hyperoxia-exposed rats receiving dexmedetomidine pretreatment with a 10 mcg/kg dose one time were found to have significantly reduced hyperoxia-induced neurodegeneration in various brain regions (p<0.001). Hyperoxia-exposed rates receiving dexmedetomidine pretreatment in single dosages of 5 mcg/kg and 10 mcg/kg had significantly decreased expression of IL-1beta protein expression than controls exposed to hyperoxia without pretreatment (p<0.01 and p<0.001, respectfully). Although these neuroprotective findings were found in hyperoxia-exposed rats, it was noted that the normoxia-exposed control group had significantly increased percentage of cells stained positive for DNA strand breakage when pretreated with one dose 10 mcg/kg dexmedetomidine (p<0.001), raising concerns for varying safety profiles in different

Oxidative stress and inflammation play a causative role in epileptogenesis and ictogenesis by taking part in neurodegeneration and excite-toxic neuronal injury (4-6). On the other hand, prolonged seizures lead to neuronal cell death by inducing mitochondrial dysfunction and incre-asing reactive oxygen species (ROS) and nitric oxide (NO). Moreover, ROS may prolong gluta-mate presence at synapses and result in further neurotoxicity (7).

Neonatal hypoxia-ischemia (HI) is a major cause of mortality and morbidity in infants and children. The most important consequences of neonatal HI is epilepsy. Epilepsy is a common neurodegenerative disorder characterized by recurrent of unprovoked seizures due to hyperexcitability and hypersynchrony of neuronal activity. Recent studies uncovered important molecular and cellular aspects of HI brain injury that may provide therapeutic target for intervening in the epileptogenesis in the developing brain. In our experiment approaches, we administrate RAGE antagonist to protect brain tissue from the effect of HI induced and inhibit apoptotic pathway and downstream products, including IL-6. Most importantly, the specific interaction between S100B

Alteration in the antioxidant components like SOD and catalase, as noticed in this study has been linked to the cellular apoptotic signaling introduced by transcriptional factors and/or mitochondrial factors. The ratio of Bax/Bcl-2 in the high dose arsenic group (50mg/L) was significantly higher than that of the control group thus initiating apoptosis in liver and brain tissues [44]. Report reveals that inorganic arsenic-induced oxidative stress can cause cellular apoptosis in the cerebrum and cerebral locations [45]. These may be the reason behind the cerebrum and cerebellum tissue disarrangement and degeneration, in our present study. Green tea extract was found to be effiecient even in the restoration of the cellular morphology and tissue

Because peroxisomes play a significant role in cell, the deficiency of peroxisomes are dangerous. One of the most life-threatening diseases which are caused by the absence of peroxisomes is Zellweger syndrome. This condition is also called peroxisome deficiency disorders. In the patients with Zellweger syndrome, there are mutations in PEX genes which encoded for peroxisome assembly. Because peroxisomes help cell oxidize the long chain fatty acids, these patients can not oxidize fatty acids and build up bile acid precursors. As a result, the symptoms or peroxisome deficiency disorder are neonatl hypotonia, neurological manifestations such as psychological and motor retardation, seizures; liver diseases such as cirrhosis, hepatomegaly… The outcome of this disease is poor. There are many infants die in the first year of life because of respiratory compromise from

Fetotoxic effects of maternal ethanol (E) intake are well documented in animals and humans. Central among the responses to E exposure are developmental deficits affecting multiple brain regions, including the cerebellum, hippocampus, olfactory bulbs, and cerebral cortex [1-4]. In vivo, moderate, clinically relevant E can generate enhanced apoptotic loss of neurons in the developing brain [4-11]. E is a prooxidant and fetal cells are highly sensitive to E/ oxidative stress (OS) [5, 12-14]. Thus, redox imbalance is a mechanism underlying E-induced neuron apoptosis in developing brain [5, 12-14]. E produces an enhanced apoptotic death in a subpopulation of cells with the lowest GSH content and normalizing this redox imbalance by stabilizing

Mechanisms of 4-HNE detoxification, clearance, and inhibition. A.) Subjection to sources of oxidative stress leads to production of ROS. These reactive species induce lipid peroxidation at cell and organelle membranes, which gives rise to a toxic byproduct: 4-HNE. This cytotoxic aldehyde is then free to form protein adducts with various targets via Michael addition, which often results in protein dysfunction and even cell death. B. & C.) Two molecules were recently identified as possible therapeutic targets for 4-HNE mediated cellular damage in hyperoxic acute lung injury. B.) Deletion of ASK1 is associated with a decrease in ROS production, which subsequently prevents formation of lipid peroxidation byproducts. C.) Knockdown of the P2X7 membrane

Since fetal environment corresponds to ~8000m altitude, prenatal defense to hypoxia consists of a long-term adaptation to limited intrauterine oxygen supply (Singer, 1999). Hence, the immature heart is more resistant to hypoxia as opposed to the adult myocardium, which may explain the significantly lower MI incidences during early ontogenetic development. In adults, cardiomyocytes are particularly susceptible to low oxygen supply and consequently hypoxia-induced cell death, whereas fetal cardiomyocytes are much more adapted (Breckenridge et al., 2013). Of all the stress that the fetus encounters, hypoxia may be the most common that affect the homeostasis of an organism, and perhaps the most clinically relevant (Malhotra et al., 1999).

The part of oxidative stress in epilepsy is additionally bolstered by studies which suggest that

The involvement of intracellular Ca2+ may be the underlying mechanism of these functional disorders. It is likely that endoplasmic reticulum disturbances are partially responsible for increasing the risk of cell death. Oxygen radicals play a part in the microvascular and parenchymal cell injury which are affiliated with organ preservation. Oxygen radicals seem to create large leakages mainly in the small venules and thus increase microvascular permeability. The hydroxyl radical, which is highly reactive, seems to be the cause of the oxygen radical production-associated microvascular alterations. While many other similar types of cell injury are triggered by an enhanced released of 02- (superoxide anion radical) or H2O2 (hydrogen peroxide), cold-induced cell injury is not. Rather, an increase in the redox-active, cellular chelatable iron pool that transforms species with low reactivity into those that are highly

Clinical research has also improved the quality of life for children and their families by conducting further studies on the standard therapies for children and improving them. As an example, in the early 1950s an epidemic of blindness in premature newborns with anoxic brain injury occurred from treatment of high dose oxygen (11). This treatment involved being placed in an environment of 100% oxygen which was assumed it would nourish the body and oxygen deficient areas instantly (12). However, later clinical research revealed that oxygen is in fact toxic to the developing retina (13) of newborns and causes blindness if left untreated. These kind of accidents in pediatric populations indicate the differences in body compositions of adults and

Oligodendrocytes are the most vulnerable brain cells to oxidative stress due to its high metabolic demand for synthesizing myelin sheaths (Ichinose et al., 2014), and relatively low levels of antioxidants (Lassmann and Van Horssen, 2011). Accumulating evidence suggests that oxidative stress plays a major role in the pathogenesis of MS. In the present study, cuprizone diet significantly increased brain TBARS level and decreased GSH content. These results are consistent with previous reports which reported that reactive oxygen species (ROS), produced as a consequence of alteration in the mitochondrial electron transport chain, have been implicated as mediators of demyelination and axonal damage in both MS and its animal models (Ghaiad et al., 2017; Kashani et al., 2014). On the other hand, treatment with linagliptin showed significant reduction in TBARS level and increase in GSH

Pregnancy is a very delicate period of time for the pregnant woman and her child. There are several factors that can interfere with the wellbeing of the baby before and after birth, and the pregnant woman. Although there are several structures and organs that protect the unborn baby, the mother needs to be careful during gestation, to protect the baby. One of the most important structures that support the embryo and fetus is the placenta. Besides its role metabolic, endocrine and immunologic functions, it is the connection between the mother and the fetus. The placenta is the organ responsible for the exchange of nourishment, oxygen and waste between them (London, Ladewig, Ball, Bindler & Cowen, 2011, p. 72). However, besides transporting the essential substances for the baby’s life, the placenta can also transport substances that can potentially harm it. Teratogen is the name for everything that, besides genetic abnormalities, can negatively affect the embryo or fetus including medications, illegal and legal drugs, viruses, bacteria, maternal antibodies, pollution, and radiation (Belsky, 2013, 50). The effects of teratogens vary according to the gestational stage of exposure, and frequency and duration of exposure. In early pregnancy or embryonic stage is the most vulnerable time of pregnancy. During this first stage of pregnancy, teratogens may inhibit implantation or lead to major structural malformation because this is when they form (Belsky, 2013, 50). The frequency and