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The literature analysis conducted in this review discusses the latest achievements in the identification of cardiovascular damage induced by oxidative stress with secondary platelet mitochondrial dysfunction. Damage to the platelets of mitochondria as a result of their interactions with reactive oxygen species (ROS) and reactive nitrogen species (RNS) can lead to their numerous ischemic events associated with hypoxia or hyperoxia processes in the cell. Disturbances in redox reactions in the platelet mitochondrial membrane lead to the direct oxidation of cellular macromolecules, including nucleic acids (DNA base oxidation), membrane lipids (lipid peroxidation process) and cellular proteins (formation of reducing groups in repair proteins and amino acid peroxides). Oxidative changes in biomolecules inducing tissue damage leads to inflammation, initiating pathogenic processes associated with faster cell aging or their apoptosis. The consequence of damage to platelet mitochondria and their excessive activation is the induction of cardiovascular and neurodegenerative diseases (Parkinson's and Alzheimer's), as well as carbohydrate metabolism disorders (diabetes). The oxidation of mitochondrial DNA can lead to modifications in its bases, inducing the formation of exocyclic adducts of the ethano and propano type. As a consequence, it disrupts DNA repair processes and conduces to premature neoplastic transformation in critical genes such as the p53 suppressor gene, which leads to the development of various types of tumors. The topic of new innovative methods and techniques for the analysis of oxidative stress in platelet mitochondria based on methods such as a nicking assay, oxygen consumption assay, Total Thrombus formation Analysis System (T-Tas), and continuous-flow left ventricular assist devices (CF-LVADs) was also discussed. They were put together into one scientific and research platform. This will enable the facilitation of faster diagnostics and the identification of platelet mitochondrial damage by clinicians and scientists in order to implement adequate therapeutic procedures and minimize the risk of the induction of cardiovascular diseases, including ischemic events correlated with them. A quantitative analysis of the processes of thrombus formation in cardiovascular diseases will provide an opportunity to select specific anticoagulant and thrombolytic drugs under conditions of preserved hemostasis., Competing Interests: The authors declare no conflicts of interest.

Radiation-induced lung injury (RILI) is a prevalent complication of thoracic tumor radiotherapy and accidental radiation exposure. Pyrroloquinoline quinone (PQQ), a novel vitamin B, plays a crucial role in delaying aging, antioxidation, anti-inflammation, and antiapoptosis. This study aims to investigate the protective effect and mechanisms of PQQ against RILI. C57BL/6 mice were exposed to a 20 Gy dose of X-ray radiation on the entire thorax with or without daily oral administration of PQQ for 2 weeks. PQQ effectively mitigated radiation-induced lung tissue damage, inflammation, oxidative stress, and epithelial cell apoptosis. Additionally, PQQ significantly inhibited oxidative stress and mitochondrial damage in MLE-12 cells. Mechanistically, PQQ upregulated the mRNA and protein levels of MOTS-c in irradiated lung tissue and MLE-12 cells. Knockdown of MOTS-c by siRNA substantially attenuated the protective effects of PQQ on oxidative stress, inflammation, and apoptosis. In conclusion, PQQ alleviates RILI by preserving mitochondrial function through a MOTS-c-dependent mechanism, suggesting that PQQ may serve as a promising nutraceutical intervention against RILI.

Mitochondria and endoplasmic reticulum (ER) are essential organelles playing pivotal roles in the regulation of cellular metabolism, energy production, and protein synthesis. In addition, these organelles are important targets susceptible to external stimuli, such as environmental pollutants. Exposure to environmental pollutants can cause the mitochondrial damage, endoplasmic reticulum stress (ERS), and oxidative stress, leading to cellular dysfunction and death. Therefore, understanding the toxic effects and molecular mechanisms of environmental pollution underlying these processes is crucial for developing effective strategies to mitigate the adverse effects of environmental pollutants on human health. In the present study, we summarized and reviewed the toxic effects and molecular mechanisms of mitochondrial damage, ERS, and oxidative stress caused by exposure to environmental pollutants as well as interactions inducing the cell apoptosis and the roles in exposure to environmental pollutants. [ABSTRACT FROM AUTHOR]

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Transient receptor potential protein (TRP) ion channels TRPA1 and TRPV1 may be important in mediating airway tissue injury and inflammation. This study was designed to clarify the role of TRPA1 and TRPV1 channels in cigarette smoke extract (CSE)-induced damage to bronchial and alveolar epithelial cells. Alveolar epithelial (A549) cells and bronchial epithelial (Beas-2B) cells were treated with CSE in the presence and absence of a TRPA1 inhibitor (100 μM, A967079), a TRPV1 inhibitor (100 μM, AMG9810) or both. DCFH-DA and MitoSOX Red probes were used to assay intracellular and mitochondrial oxidative stress, respectively. The mRNA levels of inflammatory mediators (IL-1β, IL-8, IL-18, IL-33) and antioxidants (HO-1, NQO1, MnSOD, catalase) and the protein expression levels of mitochondrial and inflammasome factors (MFN2, OPA1, DRP1, MFF, NLRP3,caspase-1) were respectively detected by RT-PCR and Western Blot. The results were validated in TRPA1 shRNA and TRPV1 shRNA cells. In both cell types, 10% CSE increased intracellular and mitochondrial oxidative stress, induced Ca2+ influx, increased inflammatory gene expression, reduced antioxidant gene expression and inhibited the activities of mitochondrial respiratory chain (MRC) complexes. 10% CSE increased the expression of mitochondrial fission proteins (MFF and DRP1), Caspase-1 and NLRP3 protein expression and decreased that of mitochondrial fusion proteins (MFN2 and OPA1). Both inhibitors and gene-knockout of TRPA1 and TRPV1 reduced oxidative stress, blocked Ca2+ influx, and inhibited inflammatory and increased antioxidant gene expression. They also prevented the changes in mitochondrial fission and fusion proteins and in MRC complexes activities induced by CSE. Both TRPA1 and TRPV1 mediate CSE-induced damage of bronchial and alveolar epithelial cells via modulation of oxidative stress, inflammation and mitochondrial damage and their inhibition should be considered as potential therapy for COPD. fx1 • TRPA1 and TRPV1 mediate CSE-induced airway epithelial cells injury. • TRPA1 and TRPV1 can modulate oxidative stress, inflammation and mitochondrial damage. • Inhibition of TRPA1and TRPV1 should be considered as potential therapy for COPD. [ABSTRACT FROM AUTHOR]

Although it is well reported that mitochondrial damage and endoplasmic reticulum (ER) stress (ERS) are involved in heavy metal-induced cytotoxicity, the role of mitochondrial damage in hexavalent chromium [Cr(VI)]-induced ERS and the correlation between the two have not been described and remain to be elucidated. The present study evaluated the ability of Cr(VI) to induce ERS in L-02 hepatocytes, and subsequently examined the role of reactive oxygen species (ROS)-mediated mitochondrial damage in Cr(VI)-induced ERS. The findings demonstrated that Cr(VI) induced ERS, which was characterized by the upregulation of ERS-associated genes and the substantial release of Ca2+ from the ER. The Cr(VI)-induced mitochondrial production of ROS, by disturbing mitochondrial respiratory chain complexes I and II, may damage mitochondria directly by inducing mitochondrial permeability transition pore opening and mitochondrial membrane potential collapse. The results additionally demonstrated that Cr(VI) induced Ca2+ release from the ER through ROS/caveolin-1/protein kinase B/inositol 1,4,5-trisphosphate receptor signaling. The application of the ROS scavenger N-acetyl-cysteine confirmed the role of ROS in Cr(VI)-mediated mitochondrial damage, ERS and apoptotic cell death. The data obtained demonstrated the role of mitochondrial damage in Cr(VI)-induced ERS and provide novel insight into the elucidation of Cr(VI)-induced cytotoxicity. [ABSTRACT FROM AUTHOR]

As lanthanide-doped sodium yttrium flouride (NaYF) nanoparticles have great potential in biomedical applications, their biosafety is important and has attracted significant attention. In the present work, three different sized NaYF:Eu nanoparticles have been prepared. Liver BRL 3A cell was used as a cell model to evaluate their biological effects. Cell viability and apoptosis assays were used to confirm the cytotoxicity induced by NaYF:Eu NPs. Apart from the elevated malondialdehyde (MDA), the decrease of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and catalase (CAT) activity indicated reactive oxygen species (ROS) generation, which were associated with oxidative damage. The decrease of mitochondrial membrane potential (MMP) value demonstrated the occurrence of mitochondria damage. Then, release of cytochrome c from mitochondria and activation of caspase-3 confirmed that NaYF:Eu NPs induced apoptosis was mitochondria damage-dependent. [ABSTRACT FROM AUTHOR]

Pharmaceuticals and personal care products are emerging environmental pollutants. Cisplatin, one of the most widely used platinum-based chemotherapeutic agents, has been found to contaminate aquatic environments. Using zebrafish embryos as a model, cisplatin was previously found to impair skin ionocytes and ion regulation. The purpose of this study was to further investigate how cisplatin damages ionocytes. Zebrafish embryos were exposed to cisplatin (0, 50, and 100 μM) for 96 h (4–100 h post-fertilization) and then stained with fluorescent dyes to reveal mitochondrial activity (rhodamine123), apoptosis (acridine orange), and oxidative stress (CellROX/MitoSOX) in ionocytes of living embryos. Results showed that cisplatin exposure decreased rhodamine 123-labeled ionocytes, induced oxidative stress in ionocytes, and promoted apoptosis in a concentration-dependent manner. Quantitative PCR analysis showed that mRNA levels of antioxidative genes (sod1 , sod2 , gpx1a , and cat) and an apoptotic gene (caps3a) were induced. In the time-course experiment at 96–98 h post-fertilization, cisplatin increased oxidative stress and apoptosis in ionocytes in a time-dependent manner. In conclusion, this study demonstrates that cisplatin exposure induces oxidative stress, mitochondrial damage, and apoptosis in ionocytes of zebrafish embryos. [Display omitted] • MitoSOX and CellROX can be used to label ROS in ionocytes of zebrafish. • Cisplatin exposure (50 and 100 μM for 96 h) induced oxidative stress and mitochondrial damage in ionocytes. • Cisplatin induced mRNA levels of antioxidative genes (sod1 , sod2 , gpx1a , and cat). • Cisplatin promoted apoptosis of ionocytes and induced mRNA level of apoptotic gene (caps3a). • This in vivo model can be applied to test drugs that have the potential to protect the cisplatin-induced renal injury. [ABSTRACT FROM AUTHOR]

Abstract: Manganese (Mn) is an essential trace element for human nutrition but also a toxicant when humans are exposed to high concentration. Occupational exposures to excess levels of Mn are known to cause manganism in humans. Mn is known to induce mitochondrial dysfunction in excessive dose, however the mechanisms underlying its action are not elucidated clearly. To determine the possible role of energy metabolism and oxidative stress in Mn-induced mitochondria injury, isolated mitochondria were exposed to different concentrations of MnCl2 (5, 50, 500, 1000μmol/L), aconitase and mitochondrial complex I activities, MDA and GSH contents, MMP were investigated. In addition, effects of NAC (500μmol/L) were studied at 500μmol/L MnCl2. Dose-dependent inhibition of aconitase and mitochondrial complex I activities, increase of MDA content, decrease of GSH content and MMP were observed. Further investigation indicated NAC pre-treatment significantly reversed toxic effect of MnCl2. The results indicated that manganese could dose-dependently induce the decline of energy metabolism and cause oxidative damage of mitochondria isolated from rat brain, and this change could be prevented by pre-treating with NAC. [Copyright &y& Elsevier]