Reduced glutathione (GSH) is the most abundant non-protein endogenous thiol. It is a ubiquitous molecule produced in most organs, but its synthesis is predominantly in the liver, the tissue in charge of storing and distributing it. GSH is involved in the detoxification of free radicals, peroxides and xenobiotics (drugs, pollutants, carcinogens, etc.), protects biological membranes from lipid peroxidation, and is an important regulator of cell homeostasis, since it participates in signaling redox, regulation of the synthesis and degradation of proteins (S-glutathionylation), signal transduction, various apoptotic processes, gene expression, cell proliferation, DNA and RNA synthesis, etc. GSH transport is a vital step in cellular homeostasis supported by the liver through providing extrahepatic organs (such as the kidney, lung, intestine, and brain, among others) with the said antioxidant. The wide range of functions within the cell in which glutathione is involved shows that glutathione’s role in cellular homeostasis goes beyond being a simple antioxidant agent; therefore, the importance of this tripeptide needs to be reassessed from a broader metabolic perspective.

According to the World Health Organization (WHO), breast cancer (BC) is the deadliest and the most common type of cancer worldwide in women. Several factors associated with BC exert their effects by modulating the state of stress. They can induce genetic mutations or alterations in cell growth, encouraging neoplastic development and the production of reactive oxygen species (ROS). ROS are able to activate many signal transduction pathways, producing an inflammatory environment that leads to the suppression of programmed cell death and the promotion of tumor proliferation, angiogenesis, and metastasis; these effects promote the development and progression of malignant neoplasms. However, cells have both non-enzymatic and enzymatic antioxidant systems that protect them by neutralizing the harmful effects of ROS. In this sense, antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), thioredoxin reductase (TrxR), and peroxiredoxin (Prx) protect the body from diseases caused by oxidative damage. In this review, we will discuss mechanisms through which some enzymatic antioxidants inhibit or promote carcinogenesis, as well as the new therapeutic proposals developed to complement traditional treatments.

Acid orange 74 (AO74) is a chromium-complex monoazo acid dye widely used in the textile industry. Due to being highly toxic and non-biodegradable, it must be removed from polluted water to protect the health of people and the environment. The aim of this study was two-fold: to evaluate the biosorption of AO74 from an aqueous solution by utilizing HCl-pretreated Lemna sp. (HPL), and to examine dye desorption from the plant material. The maximum capacity of AO74 biosorption (64.24 mg g^-1) was reached after 4 h at the most adequate pH, which was 2. The biosorption capacity decreased 25% (to 48.18 mg g^-1) during the second biosorption/desorption cycle and remained essentially unchanged during the third cycle. The pseudo-second-order kinetics model concurred well with the experimental results of assays involving various levels of pH in the eluent solution and distinct initial concentrations of AO74. NaOH (0.01 M) was the best eluent solution. The Toth isotherm model best described AO74 biosorption equilibrium data. FTIR analysis confirmed the crucial role of HPL proteins in AO74 biosorption. SEM-EDX and CLSM techniques verified the effective biosorption/desorption of the dye during the three cycles. Therefore, HPL has potential for the removal of AO74 dye from wastewaters.

High-density lipoprotein (HDL) metabolism depends on several key factors, including ATP-binding cassette (ABC) transporters such as ABCA1 and ABCG1. These transporters are essential for maintaining cholesterol homeostasis by mediating the efflux of cellular lipids and promoting HDL formation and maturation. Dysfunction in these pathways compromises HDL biogenesis, leading to lipid accumulation in macrophages and peripheral cells. Together with oxidized low-density lipoproteins (LDLs), these alterations promote foam cell formation, atherosclerotic plaque development, and the progression of cardiovascular and metabolic diseases. Oxidative stress plays a central role in disturbing lipid balance and impairing ABC transporter activity. Unlike previous reviews that have mainly summarized mechanisms of oxidative regulation, this work integrates recent molecular findings to propose a unifying framework in which oxidative stress sequentially disrupts ABCA1 and ABCG1 function, thereby altering HDL metabolism. Moreover, it highlights emerging pharmacological strategies aimed at restoring cholesterol homeostasis and mitigating oxidative damage, contributing to the prevention of cardiovascular and metabolic disorders.

Chitosan-coated magnetic nanoparticles were prepared using four different methodologies and their potentialities for DNA and Cu(II) recovery were studied. The first synthesis was done using a one-step approach, while the second one was a one-step method with pH compensation. The third methodology was done by coating the previously obtained uncoated magnetic nanoparticles and the last one was performed using glutaraldehyde as crosslinker agent after a one-step synthesis. X-Ray diffraction analysis demonstrated the crystallinity of the nanoparticles and a crystallite size between 14 and 16 nm was determined. Particle sizes between 13 and 16 nm were measured using scanning electron microscopy. The vibrational bands observed in the infrared spectrum confirmed the formation of a chitosan layer on the magnetic nanoparticles surface.The thermograms proved that the nanoparticles obtained with the first and the third methodologies resulted in particles with greater chitosan content. The highest copper adsorption capacity (22 mg/g) was obtained with the nanoparticles produced using glutaraldehyde as a crosslinker agent. The chitosan-coated nanoparticles present higher DNA adsorption capacity than the uncoated nanoparticles and the third methodology adsorbed the highest amount of DNA (27 μg).

The heart requires a continuous energy supply to sustain its unceasing contraction–relaxation cycle. Mitochondria, a double-membrane organelle, generate approximately 90% of cellular energy as adenosine triphosphate (ATP) through oxidative phosphorylation, utilizing the electrochemical gradient established by the respiratory chain. Mitochondrial function is compromised by damage to mitochondrial DNA, including point mutations, deletions, duplications, or inversions. Additionally, disruptions to proteins associated with mitochondrial membranes regulating metabolic homeostasis can impair the respiratory chain’s efficiency. This results in diminished ATP production and increased generation of reactive oxygen species. This review provides an overview of mutations affecting mitochondrial transporters and proteins involved in mitochondrial energy synthesis, particularly those involved in ATP synthesis and mobilization, and it examines their role in the pathogenesis of specific cardiomyopathies.