Calcium is used in many cellular processes and is maintained within the cell as free calcium at low concentrations (approximately 100 nM), compared with extracellular (millimolar) concentrations, to avoid adverse effects such as phosphate precipitation. For this reason, cells have adapted buffering strategies by compartmentalizing calcium into mitochondria and the endoplasmic reticulum (ER). In mitochondria, the calcium concentration is in the millimolar range, as it is in the ER. Mitochondria actively contribute to buffering cellular calcium, but if matrix calcium increases beyond physiological demands, it can promote the opening of the mitochondrial permeability transition pore (mPTP) and, consequently, trigger apoptotic or necrotic cell death. The pathophysiological implications of mPTP opening in ischemia-reperfusion, liver, muscle, and lysosomal storage diseases, as well as those affecting the central nervous system, for example, Parkinson’s disease (PD), Alzheimer’s disease (AD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS) have been reported. In this review, we present an updated overview of the main cellular mechanisms of mitochondrial calcium regulation. We specially focus on neurodegenerative diseases related to imbalances in calcium homeostasis and summarize some proposed therapies studied to attenuate these diseases.

Polycyclic aromatic hydrocarbons (PAHs) are toxic organic compounds produced during the incomplete combustion of organic materials and are commonly found in the environment due to anthropogenic activities such as industrial and vehicular emissions as well as natural sources, mainly volcanic eruptions and forest fires. PAHs are well known for their bioaccumulative capacity and environmental persistence, raising concerns due to their adverse effects on human health, including their carcinogenic potential. In recent years, bioremediation has emerged as a promising, effective, and sustainable solution for the degradation of PAHs in contaminated environments. In this context, yeasts have proven to be key microorganisms in the degradation of these compounds, owing to their ability to metabolize them through a series of enzymatic pathways. This review explores the advancements in yeast-mediated degradation of PAHs, with a particular focus on the role of enzymes such as cytochrome P450 (CYPs), epoxide hydrolases (EHs), and glutathione S-transferases (GSTs), which facilitate the breakdown of these compounds. The review also discusses the applications of genetic engineering to enhance the efficiency of yeasts in PAH degradation and the use of omics technologies to predict the catabolic potential of these organisms. Additionally, it examines studies addressing the degradation of benzo[a]pyrene (BaP) by yeasts such as Debaryomyces hansenii, and the potential future implications of omics sciences for developing new bioremediation.

Membrane blebs are released from Gram-negative bacteria, however, little is known about Brucella blebs. This work pursued two objectives, the first was to determine and identify the proteins in the membrane blebs by proteomics and in silico analysis. The second aim was to evaluate the use of membrane blebs of Brucella abortus 2308 and B. abortus RB51 as an acellular vaccine in vivo and in vitro. To achieve these aims, membrane blebs from B. abortus 2308 and RB51 were obtained and then analyzed by liquid chromatography coupled to mass spectrometry. Brucella membrane blebs were used as a “vaccine” to induce an immune response in BALB/c mice, using the strain B. abortus RB51 as a positive vaccine control. After subsequent challenge with B. abortus 2308, CFUs in spleens were determined; and immunoglobulins IgG1 and IgG2a were measured in murine serum by ELISA. Also, activation and costimulatory molecules induced by membrane blebs were analyzed in splenocytes by flow cytometry. Two hundred and twenty eight proteins were identified in 2308 membrane blebs and 171 in RB51 blebs, some of them are well-known Brucella immunogens such as SodC, Omp2b, Omp2a, Omp10, Omp16, and Omp19. Mice immunized with membrane blebs from rough or smooth B. abortus induced similar protective immune responses as well as the vaccine B. abortus RB51 after the challenge with virulent strain B. abortus 2308 (P < 0.05). The levels of IgG2a in mice vaccinated with 2308 membrane blebs were higher than those vaccinated with RB51 membrane blebs or B. abortus RB51 post-boosting. Moreover, mice immunized with 2308 blebs increased the percentage of activated B cells (CD19⁺CD69⁺) in vitro. Therefore, membrane blebs are potential candidates for the development of an acellular vaccine against brucellosis, especially those derived from the rough strains so that serological diagnostic is not affected.