Showing posts with label oxidative phosphorylation. Show all posts
Showing posts with label oxidative phosphorylation. Show all posts

Thursday, 21 March 2024

Inhaled Mica Flakes and Vitamin B12 Intercalated Clay Particles Trigger Multiple Sclerosis | Chapter 9 | New Visions in Medicine and Medical Science Vol. 1

The present study highlights about inhaled mica flakes and vitamin B12 intercalated clay particles trigger multiple sclerosis. Multiple sclerosis (MS) is the commonest devastating neurodegenerative disease in young adults in high lattitudes Soil dust containing both weathered mica particles and vitamin B12 containing clay particles (“transformation smectite“ particles) can activate myelin specific CD4+ T cells in lung. CD4+ central memory type T cell (resting phenotype) receptor is activated by soluble MHC II when it is anchored on mica particle surface and T cell adheres also on the same mica surface. Further prerequisite is that at the same time smectite clay particle intercalated with vitamin B 12 is endocytosed into the same T cell. Vitamin B12 (B12) plays a cell-autonomous role in reprogramming lymphoblasts (in this case memory B-cells and central memory T-cells). B12 affects in vivo reprogramming lymphoblasts through one carbon metabolism enhancing H3K36me3 histone methylation. T cell activation requires 1) T cell receptor activation and 2) T cell metabolic changes from oxidative phosphorylation to aerobic glycolysis. In classical activation model co-receptor B 28 activation changes T cell metabolism to oxidative glycolysis. In this case at the wrong time dosed vitamin B 12 changes T cell metabolism to oxidative glycolysis using anaplerotic feeding of TCA-cycle, permitting T cell activation to effector phenotype pathologic T cell. The hypothesis is based on new findings in immunobiology and on epidemiological observations.


Author(s) Details:

S. K. Junnila,
Health Centre of The Town of Haapajärvi, 85800 Haapajärvi, Finland.

Please see the link here: https://stm.bookpi.org/NVMMS-V1/article/view/13658

Wednesday, 9 February 2022

Study on Integrated Mitochondrial Function and Cancer-Related Fatigue in Men with Prostate Cancer Undergoing Radiation Therapy | Chapter 10 | Issues and Developments in Medicine and Medical Research Vol. 3

 Fatigue is one of the most prevalent symptoms that has the largest detrimental influence on quality of life in cancer patients, but it is also one of the least understood. The purpose of this study was to examine into changes in mitochondrial function and cancer-related fatigue in patients who were getting localised radiation therapy for non-metastatic prostate cancer (XRT).

We suggested a mitochondrial bioenergetic mechanism of radiation-induced fatigue that links defective oxidative phosphorylation (OXPHOS) via a complex III defect and ATP depletion as a result of XRT. In prostate cancer patients' peripheral blood mononuclear cells (PBMCs), integrated mitochondrial function was assessed as mitochondrial OXPHOS. The improved Piper Fatigue Scale was used to assess fatigue. Before (day 0) and after (day 21) XRT, data was collected.

At day 21 of XRT, fatigue symptoms worsened in 15 individuals with prostate cancer (p 0.05). At day 21, the rates of mitochondrial OXPHOS complex III-linked and uncoupled complex III in PBMCs were significantly lower than before XRT (p 0.05). Furthermore, a higher fatigue score was linked to a reduced OXPHOS complex III-linked respiration rate in people who had XRT.

Conclusion: At day 21 of XRT, 15 prostate cancer patients had a deficiency in oxidation commencing at complex III in their PBMC mitochondria. Complex III could be a target for pharmacological and, in particular, nutraceutical therapies in the development of CRF nursing interventions, such as coenzyme Q10.

Author(S) Details


Chao-Pin Hsiao
The Frances Payne Bolton School of Nursing, Case Western Reserve University, Cleveland, OH, USA.

Mei-Kuang Chen
Department of Psychology, University of Arizona, Tucson, AZ, USA.

Barbara Daly
The Frances Payne Bolton School of Nursing, Case Western Reserve University, Cleveland, OH, USA.

Charles Hoppel
Center for Mitochondrial Disease, Department of Pharmacology, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.

View Book:- https://stm.bookpi.org/IDMMR-V3/article/view/5471