Treatment Strategies to Reduce Mitochondrial Dysfunction and Oxidative Stress-induced Damage

Akbar Pasha^*
*Correspondence: Akbar Pasha, University Center of Excellence on Artificial Intelligence for Vision, Bandung, Indonesia, Email:

Editorial

Bipolar confusion is a constant psychological instability portrayed by a shift between craziness or hypomania and despondency. It is frequently connected with hindered usefulness. Synapse irregularity, oxidative pressure (OS), and hereditary causes is a portion of the elements that have been connected to the pathophysiology of BD. A predictable finding in BD is the presence of OS, which makes biomolecules powerless to oxidative and nitrosative harm. Dopamine (DA) levels are strikingly expanded during craziness, and DA produces receptive oxygen species (ROS) and quinones that can continue to oxidize proteins. The overproduction of ROS and receptive nitrogen species, alongside hindered upkeep of equilibrium by cell reinforcement frameworks, can bring about harm to lipids, proteins, DNA, and RNA. Likewise, the presence of ROS/ responsive nitrogen species in mitochondria prompts oxidation of mitochondrial DNA (mtDNA), proteins, and lipids. Irritation and safe brokenness might be associated with BD pathophysiology. This audit centers on the jobs of ROS and ROS-prompted oxidative harm, mitochondrial brokenness, DNA harm, and DA framework dysregulation, and safe brokenness in the pathophysiology of BD. It likewise presents an outline of expected biomarkers, including lipid peroxidation, thiobarbituric corrosive responsive substances (TBARSs), and cerebrum determined neurotrophic factor (BDNF), in patients with BD [1]. Bipolar confusion is described by mind-set changes, including intermittent hyper, hypomanic, and burdensome episodes, which might include blended side effects. In spite of the advancement in neurobiological examination, the pathophysiology of BD has not been widely depicted to date [2].

Progress in the comprehension of the neurobiology driving BD could assist with working with the disclosure of restorative targets and biomarkers for its initial recognition. Oxidative pressure (OS), which harms biomolecules and causes mitochondrial and dopamine framework dysfunctions, is a steady tracking down in patients with BD. Irritation and resistant brokenness could likewise assume a part in BD pathophysiology [3]. Explicit supplement supplements (nutraceuticals) may target neurobiological pathways recommended to be irritated in BD, like aggravation, mitochondrial brokenness, and OS. Thusly, nutraceuticals might be utilized in the adjunctive treatment of BD. This paper sums up the potential jobs of OS, mitochondrial brokenness, and resistant framework dysregulation in the beginning of BD. It then, at that point, talks about OS-moderating systems that might act as helpful mediations for BD. It likewise breaks down the connection among diet and BD as well as the utilization of healthful mediations in the treatment of BD. Likewise, it tends to the utilization of lithium treatment; novel antipsychotic specialists, including clozapine, olanzapine, risperidone, cariprazine, and quetiapine; and calming specialists to treat BD [4]. Besides, it audits the adequacy of the most involved treatments for BD, for example, mental social treatment, splendid light treatment, symbolism centered mental treatment, and electroconvulsive treatment. A superior comprehension of the jobs of OS, mitochondrial brokenness, and irritation in the pathogenesis of bipolar problem, alongside a more grounded explanation of the helpful elements of cell reinforcements, antipsychotics, mitigating specialists, lithium treatment, and light treatments, may prompt better techniques for the treatment and counteraction of bipolar issue. Major consequences of obesity are largely caused by oxidative stress. The goal of this investigation was to determine whether orlistat may lessen cardiac injury in obese animal models. For six weeks, the test rats were split into two groups and given either regular food or a high-fat diet [5]. Additionally, distilled water or no therapy was given to obese rats. Using an immunohistochemically based method and real-time PCR, the main indicators of oxidative stress, inflammation, and apoptosis were evaluated.

Through the production of free radicals and reactive oxygen species, oxidative stress may be a significant contributing factor in the development of obesity. The primary function of the enzymatic antioxidant system, which includes superoxide dismutase, glutathione peroxidase, and catalase, is to decrease free radicals and the imbalance in oxidative stress. Following nuclear factor erythroid 2-related factor-2 activation, which is essential for starting the production of antioxidant enzymes like SOD, GPx, CAT, glutathione S-transferase, heme oxygenase 1, and NAD(P)H none oxidoreductase by binding to the antioxidant response element in the promoter of genes, the cells are well-coordinated to maintain cell integrity and prevent cell damage. Inflammation is typically regarded as a key pathogenic component in the development and complications of obesity. Tumor necrosis factor (TNF) is one of the target genes for the inflammatory response that the nuclear factor kappa (NF-) family of transcription factors starts to express when it regulates the inflammatory response. After 16 weeks of HFD administration, experimental animals utilising hyperlipidemic C57/BL6 mice showed that there was myocardial inflammation present. Significant increases in the mRNA expression of pro-inflammatory cytokines like TNF- and IL-6 in the myocardium were also linked to aberrant histological changes in the myocardial tissue such cardiac fibrosis and hypertrophy. Inflammation and oxidative stress are not only connected, but an imbalance can result in cell death and serious obesityassociated problems.

Conflict of Interest

None.

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