Genotoxic effects of photodynamic therapy in laryngeal cancer cells – Anin vitrostudy

Abstract

Photodynamic therapy provides the formation of reactive oxygen species that are capable of inducing cell death. Human laryngeal carcinoma (HEp-2) cells have been evaluated in this study under PDT treatment. Cells were treated with photosensitizer aluminum phthalocyanine tetrasulfonate (AlPcS4) and irradiated with a Biopdi/Irrad-Led5 660 LED with 660 nm wavelength, intensity of delivered light of 25 mW/cm2, power of 70 mW, fluence of 5 J/cm2 for 24 h and 48 h, and then evaluated. Cell population was not increased by PDT treatment after the tested period. The apoptosis assay demonstrated that control groups exhibit approximately 60% of living cells in the 24 h and 48 h periods, however. A significant increase in apoptotic cells was observed after the photodynamic therapy treatments, for both 24 and 48 h groups. Over 50% of cells were under apoptosis after photodynamic therapy, evidencing a death process generated from the oxidative damage of the treatment. Comet assay and micronucleus assessments, both of which evaluate genotoxicity, demonstrated favorable results to damages caused by the photodynamic therapy treatment. Thus, photodynamic therapy is proposed to damage nuclear cells and the subcellular structure of carcinogenic cells. Impact statement Recently, the use of photodynamic therapy grows as an alternative treatment for cancer, since it has a noninvasive characteristic and affinity to the tumor tissue. Accordingly, understanding the therapy’s foci of action is important for the technique improvement. This work aims to understand the genotoxic effect triggered by the therapy action, thus evidencing the permanent changes caused to the genetic material of the tumor cell after the treatment. Therefore, to increase the knowledge in this study field, the methodology of the comet assay and count of micronucleus formed after the therapy was adopted in order to understand if the damage caused to the DNA of tumor cell makes its replication process unfeasible in future generations. The study allows a better therapeutic approach to the cancer treatment, making the process of association between therapies a more effective option during the disease treatment.

Aluminium phthalocyanine-mediated photodynamic therapy induces ATM-related DNA damage response and apoptosis in human oesophageal cancer cells

“…One of the key causes of cell damage and death in PDT is oxidative DNA damage, which could be induced by free radicals. DNA damage may result in single or double-strand breaks ( 35 , 47 ). When DNA damage occurs, repair mechanisms are activated to sustain the survival and stability of the DNA genome.…”

“…It functions as an upstream protein that facilitates the phosphorylation of histone H2A variant X (H2A.X) and the activation of p53 for various types of DNA repair responses ( 33 , 34 ). Previous reports have shown that phthalocyanine-based photosensitizers can induce DNA damage and cell death across multiple cancer types ( 35 , 36 ). However, the mechanism by which AlPcS 4 Cl induce DNA damage response and cell death in the oesophageal cancer cell is not clear.…”

Neuroprotective effects of taurine on SH-SY5Y cells under hydrocortisone induced stress

“…Cell viability assay evaluates the cytotoxicity of the compound employing a colorimetric test. The method consists of verifying the cell density by staining the DNA, obtaining quantitative information on the relative density of live cells adhered to culture plates, that is, obtaining indirectly the amount of DNA in the samples and consequently the number of cells present in the analyzed groups (Moraes et al, 2019).…”

“…The whole process was carried out in the dark. Data collected were statistically analyzed (Moraes et al, 2019).…”

“…They are unstable and extremely reactive molecules capable of altering other biomolecules such as proteins, carbohydrates, lipids, and nucleic acids. ROS are usually produced by body metabolism, but when they are produced in excess, they can exceed the cellular capacity for defense and repair, which leads to damage to neural cells (Moraes et al, 2019). It is evident that the chronic stress suffered by neural cells, associated with old age, predisposes to AD's development.…”