Mitophagy links oxidative stress conditions and neurodegenerative diseases

Mitophagy is activated by a number of stimuli, including hypoxia, energy stress, and increased oxidative phosphorylation activity. Mitophagy is associated with oxidative stress conditions and central neurodegenerative diseases. Proper regulation of mitophagy is crucial for maintaining homeostasis; conversely, inadequate removal of mitochondria through mitophagy leads to the generation of oxidative species, including reactive oxygen species and reactive nitrogen species, resulting in various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. These diseases are most prevalent in older adults whose bodies fail to maintain proper mitophagic functions to combat oxidative species. As mitophagy is essential for normal body function, by targeting mitophagic pathways we can improve these disease conditions. The search for effective remedies to treat these disease conditions is an ongoing process, which is why more studies are needed. Additionally, more relevant studies could help establish therapeutic conditions, which are currently in high demand. In this review, we discuss how mitophagy plays a significant role in homeostasis and how its dysregulation causes neurodegeneration. We also discuss how combating oxidative species and targeting mitophagy can help treat these neurodegenerative diseases.     

Seminal plasma vitamin B6 levels in men with asthenozoospermia and men with normal sperm motility,a measurement using liquid chromatography with tandem mass spectrometry

There is growing evidence that vitamin B₆ has a valuable contribution in maintaining normal sperm parameters; however, this contribution has not yet well-identified. Here, we aimed to measure the level of seminal plasma vitamin B₆ in men with asthenozoospermia compared to men with normal sperm motility. Ninety-seven human males with asthenozoospermia and eighty-eight human males with normal sperm motility (control) were recruited in this study. Collected semen samples were assessed for sperm motility, sperm count and semen volume. Liquid chromatography with tandem mass spectrometry was used to measure seminal plasma vitamin B₆ concentrations. A highly significant difference (p < .0001) in concentrations of seminal plasma vitamin B₆ was found between asthenozoospermic and control groups. Besides, no statistical correlations were found between seminal plasma vitamin B₆ level and sperm motility, sperm count, semen volume and men age in both tested groups. In conclusion, men with asthenozoospermia have lower seminal plasma vitamin B₆ level compared to men with normal sperm motility. Also, seminal plasma vitamin B₆ was found not to be correlated with sperm motility and count, semen volume and men age in both tested groups. These results may provide new contribution in the management of male infertility.     

Role of calcium in the regulation of mechanical power in insect flight

Most flying insect species use "asynchronous" indirect flight muscles (A-IFMs) that are specialized to generate high mechanical power at fast contraction frequencies. Unlike individual contractions of "synchronous" muscles, those of A-IFMs are not activated and deactivated in concert with neurogenically controlled cycling of myoplasmic [Ca(2+)] but rather are driven myogenically by oscillatory changes in length. The motor neurons of the A-IFMs, which fire at a rate much slower than contraction frequency, are thought to play the limited role of maintaining myoplasmic [Ca(2+)] above the critical threshold that maintains the muscle in a stretch-activatable state. Despite this asynchronous form of excitation-contraction coupling, animals can actively regulate power output as required for different flight behaviors, although the neurobiological and biophysical basis of this regulation is unknown. While presenting tethered flying fruit flies, Drosophila melanogaster, with visual stimuli, we recorded membrane potential spikes in identified A-IFM fibers. We show that mechanical power output rises and falls in concert with the firing frequency of all A-IFM fibers and cannot be explained by differential recruitment of separately innervated motor units. To explore the hypothesis that myoplasmic [Ca(2+)] might similarly rise and fall in concert with firing frequency, we genetically engineered Drosophila to express the FRET-based Ca(2+) indicator cameleon selectively within A-IFMs. The results show that Ca(2+) levels increase in proportion to muscle firing rate, both during spontaneous flight and when muscle spikes are elicited electrically. Collectively, these experiments on intact animals support an active role for [Ca(2+)] in regulating power output of stretch-activated A-IFM.