Volume 9 | Issue 4 | 1 Research Article Racheva G 1 1 Research Laboratory of Radiobiology and Radiation Protection, Military Medical Academy–Sofia, Sofia, Bulgaria. * Corresponding Author Submitted: 13 Mar 2024; Accepted: 19 Mar 2024; Published: 01 Apr 2024 Research of the Potential Radioprotective Activity of Trimethyl Glycine and N-Ace- tyl-L-Cysteine with Quantitative Analysis Using Real-Time Polymerase Chain Reac- tion (QRT-PCR) Abstract The irradiation exposure could affect the cellular genome and specifically target genes, such as TP53 gene. The TP53 gene is known as a “guardian of the genome” and is a tumor suppressor gene. Its role is to keep the cell of malignant transformation. After ionizing radiation exposure, the TP53 could mutate and the cell could continue to active proliferation (tumor cellular transformation). It has been noticed that different type of substances could have radioprotective effect and to protect the cell of malignant transformation, apoptosis, genome injuries or necrosis. Some of the natural metabolites that are proven antioxidants, show significant ability of radiation protection of the cells. The aim of that study is to analyze the possible radioprotection ability of two origin metabolites (amino acids)–trimethyl glycine (betaine) and N-acetyl-L-cysteine, applied together and in combination, first before irradiation (preventive treatment) and then 2 hours after irradiation (as a therapeutic agents). The research work is done as invitro analysis to peripheral blood cell cultures. Conclusion: The conclusion of the study is that both amino acids showed good radiation protection activity after in-vitro performed analysis. The most significant results showed the combination of both natural metabolites. Citation: Racheva G (2024) Research of the Potential Radioprotective Activity of Trimethyl Glycine and N-Acetyl-L-Cysteine with Quantitative Analysis Using Real-Time Polymerase Chain Reaction (QRT-PCR). Medical & Clinical Research 9(4), 01-05. Medical & Clinical Research Med Clin Res, 2024 ISSN: 2577 - 8005 Galina Racheva, PhD, Research Laboratory of Radiobiology and Radiation Protection, Military Medical Academy–Sofia, Sofia, Bulgaria. www.medclinres.org Keywords: TP53, QRT-PCR, cDNA, Trimethyl Glycine, Betaine, N-Acetyl-L-Cysteine, Radioprotectors, Antioxidants Introduction The function of the gene TP53 (p53) is to suppress the transformation of a normal cell into an active devided cell (tumor cellular transformation). TP53 functions as a tumor suppressor gene. It acts as a regulator of gene expression by binding to the target gene or specifically interacts with the transcription apparatuses and prevents of its transcription. The p53 gene has been defined as the “guardian of the genome”, meaning that it ensures genomic stability [1-6]. The TP53 gene could mutate in a lot of different tumor types. Hereditary predisposition to the development of oncological disease is often associated with the presence of a mutant TP53 allele [7-9]. It is suggested that the mutant TP53 allele probably blocks the action of normal, wild-type TP53 and directs the cell towards tumorigenesis [10-12] One of the cell's responses to ionizing radiation is the induction of cell cycle arrest in G1 and G2 phases. Expression of the TP53 gene increases after exposure of cells to DNA-damaging agents such as ionizing radiation. Events at the G1 phase checkpoint can be regulated by p53-dependent induction of the expression of cell cycle inhibitors. The regulation of G2-phase checkpoint events in mammalian cells has been suggested to be p53-dependent, but the mechanism of is not clarify [13,14]. Also, depending on the damage, cells can be directed to apoptosis after exposure to ionizing radiationCould be observed decrease in gene expression of the native wild-type TP53 gene, as a result of gene mutation. Increase in gene expression immediately after exposure to ionizing radiation could be as a result of p53- dependent induction of cell cycle arrest in phases G1 and possibly G2, in order to proceed with processes of repair of the resulting damages [15]. Aim The specific study aimed to determine whether, upon application of a potential radioprotector (preventive and therapeutic), irradiation with ionizing radiation and cultivation for a period longer than one cell cycle, a change in the expression of the native gene TP 53 (p53) could be observed. The decrease in the expression of the