
Medical Gas Research, Journal Year: 2024, Volume and Issue: 15(2), P. 191 - 192
Published: Dec. 7, 2024
Currently available cancer treatment options, such as surgery, chemotherapy, radiation, and immunotherapy, are limited, the results could be unsatisfactory due to systemic toxicity drug resistance. Recently, gas therapies have received widespread attention for treatment. Various gaseous molecules, nitric oxide (NO), carbon monoxide (CO), oxygen, hydrogen, hydrogen sulfide (H2S), sulfur dioxide, been studied their anticancer properties (Additional Table 1).Additional 1: Potential of different moleculesHowever, reliability implications therapy not fully understood. Precise safe methods being explored overcome operational problems difficult handling, strenuous delivery systems, low solubility in water, high tissue penetration, random diffusion body, accumulation target tissues, poisoning. In addition, mechanism most gases, including NO, H2S, CO, is concentration dependent; only gases with concentrations (≥ nM) toxic cells, while (< these may reverse protect cells.1,2 Overall, many either limited or toxic, especially advanced cases metastatic cases.3 The binding affinity hemoglobin, which poses a serious risk implementation, inhalation. Comparatively, molecular (H2) nontoxic does induce hemoglobin- related CO2, NO H2S do. High levels H2 antioxidants broad range therapeutic potential several models, lung, gallbladder, liver, brain metastasis models.4 has remarkable antioxidant neuroprotective effects other advantages, swift penetration ability cross blood–brain barrier, biomembranes, into cytosol organelles without harming healthy cells.5 can used various forms according diseases, form saline, nanocrystals. However, inhalation oral ingestion hydrogen-rich saline two common routes administration. also proposed countries safest mode administration.6,7 an easy approach Recent from cell lines animal models indicate that affect abnormal division by modulating regulatory factors tumor markers (Figure 1).6 A HeLa xenograft mouse model showed increase apoptosis rate, proliferation, oxidative stress cells. growth regulating expression overexpressed subunits transcription factors, hypoxia-inducible factor 1α nuclear factor-κΒ p65 subunit.8Figure Inhalation on tumorous normal cells.CD47: Cluster differentiation 47; CDC42: control protein 42; H2: hydrogen; ROS: reactive oxygen species.H2 inhibits 42 cluster (CD) 47 lung cells; this regulates proliferation increases susceptibility cells immune attack macrophages dendritic Similarly, promotes proinflammatory necrosis α interleukin 6.9-11 Hydrogen level p53 suppressor proteins. disrupts membrane mitochondria, induces autophagy, suppresses species cells.12 clinical study Tamana Regional Health Medical Center Japan highlighted concept improving This revealed 3 h/d improve prognosis overall survival stage IV colorectal carcinoma patients decreasing number programmed death 1/CD8+ T Factors exhausted terminal peripheral blood linked worse progression-free survival. Exhausted CD8+ usually lose immunological mitochondrial dysfunction caused inactivation peroxisome proliferator-activated receptor γ coactivator 1α, poor patients.13 Despite emerging advantages signaling molecules regulation, implementation outcomes lacking. Several uncertainties still associated reversed human lines.14 Other challenges encountered its limitedly understood mechanism, administration, targeting, utilization hazards, explosive nature.4 studies shown efficient way treat cancerous at least respiratory cancers. Another site better targeted nanocarrier-mediated delivery.15 We suggest safe, adjuvant supportive solution quality conventional because inherent biosafety potential. minimize debilitating side survival, life, parameters. Handling utilization-related issues resolved technical advancements safety precautions. independent option, significant work suggested direction. NG works River Engineering Private Limited R & D officer, all authors do any conflicts interest.
Language: Английский