Jorma Jyrkkanen, 2021-03-19, jjyrkkanen76@outlook.com ph: 1-250-859-5330
Background
After reviewing the work of Sameer Calghatgi et al 2013 it became clear to me that the antibiotic production of ROS and Lipid Peroxide were the byproducts of antibiotics on mitochondria with potential CARDIOLOGY outcomes. From only a preliminary cursory examination of a few of the thousands of genes involved in heart function that are potentially impacted by ROS and LP I found the following potential routes for their impacts on heart and coronary artery diseases which need detailed and close examination with each and every antibiotic in use. I based the cardiology impacts on predictions arising from this work. https://www.heighpubs.org/jccm/pdf/jccm-aid1104.pdf
1. Oxidative damage to DNA, membranes, lipids and proteins, alteration of gene expression
2. Lipid Peroxide
3. Rupture of mitochondria
4. Mutations in mitochondrial proteins and peptides
5. Mutation of heart function genes and probable epigenetic alteration of genes
6. Loss or damage to mitochondria integrity and reproduction essential for heart energy supply
7. Dysbiosis linked issues of pathogenic substances and signalling
8. Inflammation and athersclerosis
9. Damage associated molecular pattern molecules (DAMPs) that are released during condition of oxidative stress.
10. Redox stress leading to release of DAMPs triggering TLR4-mediated inflammation and organ injury.
11. Cardiovascular diseases associated with increases in IL-6, such as atherosclerosis and hypertension, are also associated with oxidative stress, particularly increases in vascular superoxide, suggesting a potential relationship between superoxide, IL-6 and arterial pressure.
12. Interleukin-6 (IL-6) has been emphasized by reports of elevated circulating as well as intracardiac IL-6 levels in patients with congestive heart failure (CHF). IL-6 may contribute to the progression of myocardial damage and dysfunction in chronic heart failure syndrome resulting from different causes
13. ROS at low concentrations have important functions in regulating pathways such as TNFR1 signaling, but high ROS concentrations ultimately lead to DNA damage and cell death. TNF modulates both cardiac contractility and peripheral resistance, the two most important haemodynamic determinants of cardiac function
14. DNA Damage Response/TP53 Pathway Is Activated and Contributes to the Pathogenesis of Dilated Cardiomyopathy Associated With LMNA (Lamin A/C) Mutations
15. Increased ROS generation and reduction in ATP level, contributing to ATP-producing disorders and oxidative stress, which may further accelerate development or vulnerability of atherosclerosis and myocardial ischemic injury
16. Dysregulated ROS production and oxidative stress have been implicated in a host of cardiac diseases, including cardiac hypertrophy, heart failure (HF), cardiac ischemia–reperfusion injury (IRI), and diabetic cardiomyopathy
17. HNE a breakdown product of LP can trigger cardiovascular pathology by inflammation. LP linked to atherogenesis.
18. Dysbiosis triggers immune depression opening door to pathogenic viruses, bacteria, microbial toxins which may also pose a risk to neurological intereference in vagal nerve signalling.
19. Depression of TP53 TSG function affects OP and ATP, antioxidant regulation and stability, programmed senescence
20. Epigenetic effects on cardiology important genes undetermined. Ex; Silencing, turning on when not supposed to, over expression
Reference
Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells
By Sameer Kalghatgi, Catherine S. Spina, James C. Costello, Marc Liesa, J. Ruben Morones-Ramirez, Shimyn Slomovic, Anthony Molina, Orian S. Shirihai, James J. Collins. Science Translational Medicine03 Jul 2013 : 192ra85. Mitochondrial dysfunction and oxidative damage induced by bactericidal antibiotics in mammalian cells may be alleviated by an antioxidant or prevented by preferential use of bacteriostatic antibiotics.
Environment Gene Interactions 