Redox regulation participates in the control of various aspects of metabolism. Reactive oxygen and nitrogen species participate in many reactions under physiological conditions. When these species overcome the antioxidant defense system, a distressed status emerges, increasing biomolecular damage and leading to functional alterations. Air pollution is one of the exogenous sources of reactive oxygen and nitrogen species. Ambient airborne particulate matter (PM) is important because of its complex composition, which includes transition metals and organic compounds. Once in contact with the lungs’ epithelium, PM components initiate the synthesis of inflammatory mediators, macrophage activation, modulation of gene expression, and the activation of transcription factors, which are all related to the physiopathology of chronic respiratory diseases, including cancer. Even though the pathophysiological pathways that give rise to the development of distress and biological damage are not fully understood, scientific evidence indicates that redox-dependent signaling pathways are involved. This article presents an overview of the redox interaction of air pollution inside the human body and the courses related to chronic respiratory diseases.

Background: Coronavirus infectious disease 2019 (COVID-19) is a significant public health problem worldwide. COVID-19 increases the risk of non-pulmonary complications such as acute myocardial injury, renal failure, thromboembolic events, and multi-organic damage. Several studies have documented increased inflammation molecules, endothelial dysfunction biomarkers, and dysregulation of coagulation factors in COVID-19 patients. In addition, endothelium dysfunction is exacerbated by the oxidative stress (OxS) promoted by endocrine and cardiovascular molecules. Our objective was to evaluate whether endothelial and OxS biomarkers were associated with mortality in hospitalized COVID-19 patients. Methods: A prospective cohort study was performed. Patients ≥18 years old with confirmed COVID-19 that required hospitalization were included in a prospective cohort study. Endothelium and oxidative stress biomarkers were collected between 3 and 5 days after admission. Results: A total of 165 patients were evaluated; 56 patients succumbed. The median follow-up was 71 days [23–129]. Regarding endothelial dysfunction and OxS biomarkers, patients who did not survive had higher levels of nitrates (0.4564 [0.1817–0.6761] vs. 0.2817 [0.0517–0.5], p = 0.014), total nitrates (0.0507 [−0.0342–0.1809] vs. −0.0041 [−0.0887–0.0909], p = 0.016), sE-Selectin (1.095 [0.86–1.495] vs. 0.94 [0.71–1.19], p = 0.004), and malondialdehyde (MDA) (0.50 [0.26–0.72] vs. 0.36 [0.23–0.52], p = 0.010) compared to patients who survived. Endothelial and OxS biomarkers independently associated with mortality were sE-selectin (HR:2.54, CI95%; from 1.11 to 5.81, p = 0.027), nitrates (HR:4.92, CI95%; from 1.23 to 19.63, p = 0.024), and MDA (HR: 3.05, CI95%; from 1.14 to 8.15, p = 0.025). Conclusions: Endothelial dysfunction (sE-selectin and nitrates) and OxS (MDA) are independent indicators of a worse prognosis in COVID-19 patients requiring hospitalization.

Particulate matter pollution has been particularly linked to respiratory diseases. Particles ≤ 2.5 µm in aerodynamic diameter (PM_2.5) easily penetrate the lower airways of the lungs and release constituents that produce local or systemic effects by translocation. Bioaccessibility refers to the availability of metals when dissolved in body fluids in vitro. Given that the biological composition of lung fluids facilitates the bioaccessibility of PM_2.5 components, we identified the soluble elements in the following artificial fluids: Gamble´s solution, artificial interstitial fluid (AIF), simulated epithelial lung fluid (SELF), artificial lysosomal fluid (ALF), and deionized water. We collected PM_2.5 from three sites in Mexico City (CDMX), Pedregal (PED), Universidad Autónoma Metropolitana Iztapalapa (UIZ), and the Laboratory of Environmental Analysis (LAA), during two seasons, dry-hot (dh) and dry-cold (dc). The PM_2.5 was sonicated and incubated in each fluid for 24 h at 37 °C and then centrifuged. We measured the metal (loid) content in the supernatant by ICP-MS. Bioaccessibility, in terms of element concentration and number of elements detected, was (from higher to lower) as follows: LAA > UIZ > PED; dh > dc; and ALF > SELF > Water > AIF > Gamble´s solution. The metal (loid)s with the highest levels were Zn, As, Cr, and V. In conclusion, metal (loid)s are differentially soluble in various solutions, and the time it takes to read the solutions affects the bioaccessibility results from each fluid when the samples are not acidified (no digestion).

There are several methods to assess the function of the autonomic nervous system. Among them, heart rate recovery (HRR) is an accepted, easy, low-cost technique. Different pathological conditions have been related to the development of autonomic dysfunction. Our study aimed to evaluate the relationship between HRR and HRR-derived parameters in ambulatory patients with asthma or type 2 diabetes followed at the National Institutes of Health in Mexico City. A total of 78 participants, 50 women and, 28 men were enrolled; anthropometric, respiratory evaluations, and fasting blood samples were taken before participants performed a 6-min walking test (6MWT). Abnormal HRR was defined as a drop of ≤8 and ≤11 beats/min at 1 or 2 min and correlated negatively with basal oxygen saturation at 1 min. Heart rate at 1 min, correlated negatively with final oxygen saturation (p < 0.01). Statistically significant negative correlations were also observed between red cell count and white blood cell count and HOMA-IR with a p < 0.01. Since discrete hematological but significant changes correlated with HRR and HRR-derived parameters, we consider that these measures are helpful in clinical settings to identify subclinical autonomic dysfunction that permits us to prevent or anticipate chronic and fatal clinical outcomes.

Knee osteoarthritis (OA) is a leading cause of disability worldwide. Oxidative stress (OS), enhanced by exposure to heavy metals such as cadmium (Cd), may contribute to its progression. Cd, present in tobacco smoke, disrupts chondrocyte viability, redox balance, and essential metal homeostasis. This study aimed to determine whether Cd exposure, particularly through smoking, influences the development and severity of knee OA by affecting antioxidant defense, metallothioneins (MTs) expression, arginase II activity, and trace metal levels in blood, synovial fluid (SF), and cartilage. Fifty-one OA patients were stratified by smoking status (non-smokers, ex-smokers, smokers). Cd and other metals were quantified by ICP-MS, along with OS markers (MDA, MGO, AOPPs), antioxidant enzymes (GST, GGT, CAT), prooxidant enzymes (MPO, arginase II), and metallothinein-1A and 2A (MT-1A/2A) levels. Non-parametric tests assessed correlations between Cd and redox markers. Smokers exhibited higher Cd in blood (0.34 ng/mL) and cartilage (26.07 ng/g), with increased GST, GGT, MDA, and AOPPs. Cd correlated positively with MDA (rho = 0.319, P = 0.033). In SF, elevated CAT, GGT, and arginase II activity were found in patients with high Cd levels (Q3), alongside increased MT-2A expression in smokers (P = 0.018). Cd exposure was also linked to an imbalance of essential metals such as selenium (Se). These findings suggest that Cd, mainly from smoking, exacerbates OS, alters redox enzyme activity, induces MT-2A, and disrupts metal homeostasis, potentially mediating OA pathogenesis. Longitudinal studies are warranted to confirm its causal role in disease progression.

Background: Post-COVID-19 syndrome is associated with endothelial dysfunction (ED) and various sequelae, particularly in individuals who experienced critical illness during the acute phase, affecting lung function and the musculoskeletal system. L-citrulline, a nonessential amino acid, has been shown to improve endothelial function, systemic inflammation, blood pressure, and physical performance. This study aimed to assess the effects of L-citrulline supplementation on ED and body composition in patients with post-COVID-19 syndrome. Methods: We conducted an open-label randomized controlled clinical trial at the Instituto Nacional de Enfermedades Respiratorias in Mexico City, Mexico, from February 2021 to May 2022. Eligible subjects were adults aged ≥18 years who recovered from COVID-19 and required hospitalization during acute COVID-19. Participants were randomized 1:1 into two groups: (1) the L-citrulline group (4 g/day) and (2) the control group. The intervention lasted three months. Endothelial-related biomarkers, including endothelin-1, sE-selectin, ICAM-1, and VCAM-1, were investigated. Body composition was measured using electrical bioimpedance, and aerobic capacity was assessed with the 6 min walk test (6MWT). Treatment effects were analyzed using two-way repeated-measures ANOVA (group × time). Results: In total, 43 subjects participated in the study. After three months of follow-up, the intervention group showed a decrease in ICAM-1 (−32.59 ng/mg of protein; 95% CI −52.85 to −12.33 vs. −2.31 ng/mg of protein, CI 95%: −21.59 to 16.95, p = 0.034) and an increase in 6MWT (141.2 m; 95% CI: 98.40 to 184 vs. 67.70 m, CI 95%: 30.62 to 104.78, p = 0.011) compared with the control group. No differences in body composition were observed between the groups at follow-up. Conclusions: L-citrulline supplementation for three months decreased ICAM-1 and increased 6MWT.