The APE1/REF-1 and the hallmarks of cancer.

APE1/REF-1 (apurinic/apyrimidinic endonuclease 1 / redox factor-1) is a protein with two domains, with endonuclease function and redox activity. Its main activity described is acting in DNA repair by base excision repair (BER) pathway, which restores DNA damage caused by oxidation, alkylation, and single-strand breaks. In contrast, the APE1 redox domain is responsible for regulating transcription factors, such as AP-1 (activating protein-1), NF-κB (Nuclear Factor kappa B), HIF-1α (Hypoxia-inducible factor 1-alpha), and STAT3 (Signal Transducers and Activators of Transcription 3). These factors are involved in physiological cellular processes, such as cell growth, inflammation, and angiogenesis, as well as in cancer. In human malignant tumors, APE1 overexpression is associated with lung, colon, ovaries, prostate, and breast cancer progression, more aggressive tumor phenotypes, and worse prognosis. In this review, we explore APE1 and its domain's role in cancer development processes, highlighting the role of APE1 in the hallmarks of cancer. We reviewed original articles and reviews from Pubmed related to APE1 and cancer and found that both domains of APE1/REF-1, but mainly its redox activity, are essential to cancer cells. This protein is often overexpressed in cancer, and its expression and activity are correlated to processes such as proliferation, invasion, inflammation, angiogenesis, and resistance to cell death. Therefore, APE1 participates in essential processes of cancer development. Then, the activity of APE1/REF-1 in these hallmarks suggests that targeting this protein could be a good therapeutic approach.

Effects of low­power red laser and blue LED on mRNA levels from DNA repair genes in human breast cancer cells.

Photobiomodulation (PBM) induced by non-ionizing radiations emitted from low-power lasers and light-emitting diodes (LEDs) has been used for various therapeutic purposes due to its molecular, cellular, and systemic effects. At the molecular level, experimental data have suggested that PBM modulates base excision repair (BER), which is responsible for restoring DNA damage. There is a relationship between the misfunction of the BER DNA repair pathway and the development of tumors, including breast cancer. However, the effects of PBM on cancer cells have been controversial. Breast cancer (BC) is the main public health problem in the world and is the most diagnosed type of cancer among women worldwide. Therefore, the evaluation of new strategies, such as PBM, could increase knowledge about BC and improve therapies against BC. Thus, this work aims to evaluate the effects of low-power red laser (658 nm) and blue LED (470 nm) on the mRNA levels from BER genes in human breast cancer cells. MCF-7 and MDA-MB-231 cells were irradiated with a low-power red laser (69 J cm-2, 0.77 W cm-2) and blue LED (482 J cm-2, 5.35 W cm-2), alone or in combination, and the relative mRNA levels of the APTX, PolB, and PCNA genes were assessed by reverse transcription-quantitative polymerase chain reaction. The results suggested that exposure to low-power red laser and blue LED decreased the mRNA levels from APTX, PolB, and PCNA genes in human breast cancer cells. Our research shows that photobiomodulation induced by low-power red laser and blue LED decreases the mRNA levels of repair genes from the base excision repair pathway in MCF-7 and MDA-MB-231 cells.

Could violet-blue lights increase the bacteria resistance against ultraviolet radiation mediated by photolyases?

Studies have demonstrated bacterial inactivation by radiations at wavelengths between 400 and 500 nm emitted by low-power light sources. The phototoxic activity of these radiations could occur by oxidative damage in DNA and membrane proteins/lipids. However, some cellular mechanisms can reverse these damages in DNA, allowing the maintenance of genetic stability. Photoreactivation is among such mechanisms able to repair DNA damages induced by ultraviolet radiation, ranging from ultraviolet A to blue radiations. In this review, studies on the effects of violet and blue lights emitted by low-power LEDs on bacteria were accessed by PubMed, and discussed the repair of ultraviolet-induced DNA damage by photoreactivation mechanisms. Data from such studies suggested bacterial inactivation after exposure to violet (405 nm) and blue (425-460 nm) radiations emitted from LEDs. However, other studies showed bacterial photoreactivation induced by radiations at 348-440 nm. This process occurs by photolyase enzymes, which absorb photons at wavelengths and repair DNA damage. Although authors have reported bacterial inactivation after exposure to violet and blue radiations emitted from LEDs, pre-exposure to such radiations at low fluences could activate the photolyases, increasing resistance to DNA damage induced by ultraviolet radiation.

Photobiomodulation at molecular, cellular, and systemic levels.

Since the reporting of Endre Mester's results, researchers have investigated the biological effects induced by non-ionizing radiation emitted from low-power lasers. Recently, owing to the use of light-emitting diodes (LEDs), the term photobiomodulation (PBM) has been used. However, the molecular, cellular, and systemic effects involved in PBM are still under investigation, and a better understanding of these effects could improve clinical safety and efficacy. Our aim was to review the molecular, cellular, and systemic effects involved in PBM to elucidate the levels of biological complexity. PBM occurs as a consequence of photon-photoacceptor interactions, which lead to the production of trigger molecules capable of inducing signaling, effector molecules, and transcription factors, which feature it at the molecular level. These molecules and factors are responsible for cellular effects, such as cell proliferation, migration, differentiation, and apoptosis, which feature PBM at the cellular level. Finally, molecular and cellular effects are responsible for systemic effects, such as modulation of the inflammatory process, promotion of tissue repair and wound healing, reduction of edema and pain, and improvement of muscle performance, which features PBM at the systemic level.

Effects of photobiomodulation by low-power lasers and LEDs on the viability, migration, and invasion of breast cancer cells.

Among the malignant tumors, breast cancer is the most commonly diagnosed worldwide, being the most prevalent in women. Photobiomodulation has been used for wound healing, swelling and pain reduction, and muscle repair. The application of photobiomodulation in cancer patients has been controversial. Therefore, a better understanding of radiation-induced effects involved in photobiomodulation on cancer cells is needed. Thus, this study aimed to investigate the effects of exposure to low-power lasers and LEDs on cell viability, migration, and invasion in human breast cancer cells. MCF-7 and MDA-MB-231 cells were irradiated with a low-power red laser (23, 46, and 69 J/cm2, 0.77 W/cm2) and blue LED (160, 321, and 482 J/cm2, 5.35 W/cm2), alone or in combination. Cell viability was assessed using the WST-1 assay, cell migration was evaluated using the wound healing assay, and cell invasion was performed using the Matrigel transwell assay. Viability and migration were not altered in MCF-7 and MDA-MB-231 cultures after exposure to low-power red laser and blue LED. However, there was a decrease in cell invasion from the cultures of the two cell lines evaluated. The results suggest that photobiomodulation induced by low-power red laser and blue LED does not alter cell viability and migration but decreases cell invasion in human breast cancer cells.

Low-power infrared laser modulates mRNA levels from genes of base excision repair and genomic stabilization in heart tissue from an experimental model of acute lung injury.

The aim of this study was to evaluate photobiomodulation effects on mRNA relative levels from genes of base excision repair and genomic stabilization in heart tissue from an experimental model of acute lung injury by sepsis. For experimental procedure, animals were randomly assigned to six main groups: (1) control group was animals treated with intraperitoneal saline solution; (2) LASER-10 was animals treated with intraperitoneal saline solution and exposed to an infrared laser at 10 J cm-2; (3) LASER-20 was animals treated with intraperitoneal saline solution and exposed to an infrared laser at 20 J cm-2; (4) acute lung injury (ALI) was animals treated with intraperitoneal LPS (10 mg kg-1); (5) ALI-LASER10 was animals treated with intraperitoneal LPS (10 mg kg-1) and, after 4 h, exposed to an infrared laser at 10 J cm-2 and (6) ALI-LASER20 was animals treated with intraperitoneal LPS (10 mg kg-1) and, after 4 h, exposed to an infrared laser at 20 J cm-2. Irradiation was performed only once and animal euthanasias for analysis of mRNA relative levels by RT-qPCR. Our results showed that there was a reduction of mRNA relative levels from ATM gene and an increase of mRNA relative levels from P53 gene in the heart of animals with ALI when compared to the control group. In addition, there was an increase of mRNA relative levels from OGG1 and APE1 gene in hearts from animals with ALI when compared to the control group. After irradiation, an increase of mRNA relative levels from ATM and OGG1 gene was observed at 20 J cm-2. In conclusion, low-power laser modulates the mRNA relative levels from genes of base excision repair and genomic stabilization in the experimental model of acute lung injury evaluated.

Low-power therapeutic lasers on mRNA levels.

Gene expression evaluation in cells and biological tissues has been crucial for research in biology, medicine, biotechnology, and diagnostic. Messenger ribonucleic acid (mRNA) levels show relationship with gene expression, and they can be measured by real-time quantitative polymerase chain reaction (RT-qPCR) for the quantification of steady-state mRNA levels in cells and biological tissues. Radiations emitted from low-power lasers induce photobiomodulation, which is the base of therapeutic protocols for disease treatment. Despite that the understanding on photobiomodulation has been improved by mRNA level evaluation, laser irradiation parameters and procedures are diversified among studies, harming the comparison of RT-qPCR data. In this systematic review, data from mRNA levels reported in photobiomodulation studies were summarized regarding the process, function, and gene. Literature search was conducted for the assessment of published reports on mRNA levels evaluated by RT-qPCR in cells and biological tissues exposed to low-power lasers. Data showed that mRNA levels have been evaluated by RT-qPCR for a variety of genes related to molecular, cellular, and systemic processes after low-power violet-orange, red, and infrared laser exposure. Results from gene expression have increased the understanding of the mechanisms involved in photobiomodulation, and they can be useful to increase the efficacy and safety of clinical applications based on low-power lasers.

Low-power infrared laser modulates telomere length in heart tissue from an experimental model of acute lung injury.

Acute lung injury and acute respiratory distress syndrome can occur as a result of sepsis. Cardiac dysfunction is a serious component of multi-organ failure caused by severe sepsis. Telomere shortening is related to several heart diseases. Telomeres are associated with the shelterin protein complex, which contributes to the maintenance of telomere length. Low-power infrared lasers modulate mRNA levels of shelterin complex genes. This study aimed to evaluate effects of a low-power infrared laser on mRNA relative levels of genes involved in telomere stabilization and telomere length in heart tissue of an experimental model of acute lung injury caused by sepsis. Animals were divided into six groups, treated with intraperitoneal saline solution, saline solution and exposed to a low-power infrared laser at 10 J cm-2 and 20 J cm-2, lipopolysaccharide (LPS), and LPS and, after 4 h, exposed to a low-power infrared laser at 10 J cm-2 and 20 J cm-2. The laser exposure was performed only once. Analysis of mRNA relative levels and telomere length by RT-qPCR was performed. Telomere shortening and reduction in mRNA relative levels of TRF1 mRNA in heart tissues of LPS-induced ALI animals were observed. In addition, laser exposure increased the telomere length at 10 J cm-2 and modulated the TRF1 mRNA relative levels of at 20 J cm-2 in healthy animals. Although the telomeres were shortened and mRNA levels of TRF1 gene were increased in nontreated controls, the low-power infrared laser irradiation increased the telomere length at 10 J cm-2 in cardiac tissue of animals affected by LPS-induced acute lung injury, which suggests that telomere maintenance is a part of the photobiomodulation effect induced by infrared radiation.

Hypoxia effects on cancer stem cell phenotype in colorectal cancer: a mini-review.

Colorectal cancer (CRC) is ranked third most incident and second most deadly around the world, and even though treatments significantly developed over the years, overall survival remains low. This scenario has the contribution of cancer stem cells (CSC), a subpopulation of the heterogeneous tumor bulk, considered to be responsible for the tumor maintenance, conventional therapies resistance, metastasis, and recurrence. In this regard, hypoxia appears as an important component of tumor microenvironment and CSC niche, being associated with a worse prognosis. Therefore, it is vital the study of hypoxia influence on CSC phenotype in CRC. The aim of this mini-review article is to present a brief overview on this field. Recent articles discoursed about CSC molecular regulation, signalling pathways, methods for the study of the topic, as well as molecules and drugs capacity of inhibiting the interplay of hypoxia-CSC. Finally, the studies demonstrated important results, extensively accessing the topics of cellular and molecular regulation and therapeutic intervention, being morphology an area to be more explored.

5-Aza-2'-deoxycytidine induces a greater inflammatory change, at the molecular levels, in normoxic than hypoxic tumor microenvironment.

Hypoxia is associated with tumor aggressiveness and poor prognosis, including breast cancer. Low oxygen levels induces global genomic hypomethylation and hypermethylation of specific loci in tumor cells. DNA methylation is a reversible epigenetic modification, usually associated with gene silencing, contributing to carcinogenesis and tumor progression. Since the effects of DNA methyltransferase inhibitor are context-dependent and as there is little data comparing their molecular effects in normoxic and hypoxic microenvironments in breast cancer, this study aimed to understand the gene expression profiles and molecular effects in response to treatment with DNA methyltransferase inhibitor in normoxia and hypoxia, using the breast cancer model. For this, a cDNA microarray was used to analyze the changes in the transcriptome upon treatment with DNA methyltransferase inhibitor (5-Aza-2'-deoxycytidine: 5-Aza-2'-dC), in normoxia and hypoxia. Furthermore, immunocytochemistry was performed to investigate the effect of 5-Aza-2'-dC on NF-κB/p65 inflammation regulator subcellular localization and expression, in normoxia and hypoxia conditions. We observed that proinflammatory pathways were upregulated by treatment with 5-Aza-2'-dC, in both conditions. However, treatment with 5-Aza-2'-dC in normoxia showed a greater amount of overexpressed proinflammatory pathways than 5-Aza-2'-dC in hypoxia. In this sense, we observed that the NF-κB expression increased only upon 5-Aza-2'-dC in normoxia. Moreover, nuclear staining for NF-κB and NF-κB target genes upregulation, IL1A and IL1B, were also observed after 5-Aza-2'-dC in normoxia. Our results suggest that 5-Aza-2'-dC induces a greater inflammatory change, at the molecular levels, in normoxic than hypoxic tumor microenvironment. These data may support further studies and expand the understanding of the DNA methyltransferase inhibitor effects in different tumor contexts.

Low-power lasers on bacteria: stimulation, inhibition, or effectless?

Clinical protocols based on low-power lasers have been widely used for inflammation process resolution improvement, pain relief, wound healing, and nerve regeneration. However, there are concerns if exposure to such lasers could have negative effects on infected organs and tissues. There are experimental data suggesting exposure to radiations emitted by low-power lasers either induces stimulation, inhibition, or it is effectless on bacterial cultures. Thus, this review aimed to carry out a review of studies and to propose a hypothesis to explain why exposure to low-power lasers could stimulate, inhibit, or have no effect on bacteria. A literature search was carried out for assessment of published reports on effect of low-power lasers on bacteria. The experimental data suggest that keys for determining laser-induced effects on bacteria are specific physical laser and biological parameters. Final consequence on bacterial cells could depend on exposure to low-power laser which could either cause more stimulation of endogenous photoacceptors, more excitation of endogenous photosensitizers, or a balance between such effects.

Effect of low power lasers on prokaryotic and eukaryotic cells under different stress condition: a review of the literature.

Radiations emitted by low power radiation sources have been applied for therapeutic proposals due to their capacity of inactivating bacteria and cancer cells in photodynamic therapy and stimulating tissue cells in photobiomodulation. Exposure to these radiations could increase cell proliferation in bacterial cultures under stressful conditions. Cells in infected or not infected tissue injuries are also under stressful conditions and photobiomodulation-induced regenerative effect on tissue injuries could be related to effects on stressed cells. The understanding of the effects on cells under stressful conditions could render therapies based on photobiomodulation more efficient as well as expand them. Thus, the objective of this review was to update the studies reporting photobiomodulation on prokaryotic and eukaryotic cells under stress conditions. Exposure to radiations emitted by low power radiation sources could induce adaptive responses enabling cells to survive in stressful conditions, such as those experienced by bacteria in their host and by eukaryotic cells in injured tissues. Adaptive responses could be the basis for clinical photobiomodulation applications, either considering their contraindication for treatment of infected injuries or indication for treatment of injuries, inflammatory process resolution, or tissue regeneration.

Photobiomodulation by dual-wavelength low-power laser effects on infected pressure ulcers.

The aim of this study was to evaluate the effects of photobiomodulation (PBM) by dual-wavelength low-power lasers on the healing and bacterial bioburden of pressure ulcer (PU) models. Twenty-five male Swiss mice were divided into five equal groups. Ischemia reperfusion cycles were employed to cause PU formation by the external application of magnetic plates. Immediately after wounding, a suspension of Pantoea agglomerans was applied at the base of all the wounds of the infected groups, using a calibrated pipette. PBM (simultaneous emission at 660 and 808 nm, 142.8 J/cm2, in continuous wave emission mode) was applied to the PUs for 14 sessions. The animals were euthanized 14 days after PU induction, and their tissues were analyzed for wound contraction and reepithelialization, epidermis thickness, bacterial survival, and IL-1ß and IL-10 mRNA level evaluations. The PU areas appeared larger in the mice from the infected groups than in those in the laser group 4 days after PU induction and presented incomplete reepithelialization 14 days after PU induction. However, the PBM accelerated the wound healing in the infected + laser group compared with the infected group 11 and 14 days following the PU induction. The infected and irradiated PUs exhibited a thinner neo-epidermis than those in the infected group, and the bacterial survival decreased in the laser group; the relative expression IL-1ß mRNA levels demonstrated an increasing tendency while the relative expression IL-10 mRNA levels demonstrated a decreasing tendency in the infected + laser and laser groups. These results suggest that PBM improves healing by killing or inhibiting bacteria in PUs as well as by accelerating the wound healing, resulting in tissue repair.

Correction to: Photobiomodulation by dual-wavelength low-power laser effects on infected pressure ulcers.

The author name Maria Maria Côrtes Thomé Lima was incorrectly captured in the original article. The correct author name should be Andrezza Maria Côrtes Thomé Lima. The original article has been corrected.

Low-power laser alters mRNA levels from DNA repair genes in acute lung injury induced by sepsis in Wistar rats.

Acute lung injury (ALI) is defined as respiratory failure syndrome, in which the pathogenesis could occur from sepsis making it a life-threatening disease by uncontrolled hyperinflammatory responses. A possible treatment for ALI is the use of low-power infrared lasers (LPIL), whose therapeutical effects depend on wavelength, power, fluence, and emission mode. The evaluation mRNA levels of repair gene related to oxidative damage after exposure to LPIL could provide important information about the modulation of genes as treatment for ALI. Thus, the aim of this study was to evaluate the mRNA levels from OGG1, APEX1, ERCC2, and ERCC1 genes in lung tissue from Wistar rats affected by ALI and after exposure to LPIL (808 nm; 100 mW). Adult male Wistar rats (n = 30) were randomized into six groups (n = 5, for each group): control, 10 J/cm2 (2 J), 20 J/cm2 (5 J), ALI, ALI + LPIL 10 J/cm2 and ALI + LPIL 20 J/cm2. ALI was induced by intraperitoneal E. coli lipopolysaccharide injection (10 mg/kg). Lungs were removed, and samples were withdrawn for total RNA extraction, cDNA synthesis, and mRNA levels were evaluated by RT-qPCR. Data normality was verified by Kolmogorov-Smirnov, comparisons among groups were by Student's t test, Mann-Whitney test, one-way ANOVA, Kruskal-Wallis followed by post-tests. Data showed that OGG1 (0.39 ± 0.10), ERCC2 (0.67 ± 0.24), and ERCC1 (0.60 ± 0.19) mRNA levels are reduced in ALI group when compared with the control group (1.00 ± 0.07, 1.03 ± 0.25, 1.01 ± 0.16, respectively) and, after LPIL, mRNA relative levels from DNA repair genes are altered when compared to non-exposed ALI group. Our research shows that ALI alter mRNA levels from genes related to base and nucleotide excision repair genes, suggesting that DNA repair is part of cell response to sepsis, and that photobiomodulation could modulate the mRNA levels from these genes in lung tissue.

The orally active pterocarpanquinone LQB-118 exhibits cytotoxicity in prostate cancer cell and tumor models through cellular redox stress.

BACKGROUND: The targeted induction of reactive oxygen species (ROS) is a developing mechanism for cancer therapy. LQB-118 is a pterocarpanquinone and ROS-inducing agent with proven antineoplastic activity. Here, LQB-118 efficacy and mechanism of activity, were examined in Prostate Cancer (PCa) cell and tumor models. METHODS: PC3, LNCaP, and LAPC4 PCa cells were applied. Dicoumarol treatment was used to inhibit quinone reductase activity. N-acetylcysteine (NAC) was applied as a ROS scavenger. ROS production was quantified by H2 DCFDA flow cytometry. LQB-118 treated cells were evaluated for changes in lipid peroxidation, viability, and apoptosis. Treatment-induced gene expression was measured by RT-qPCR and Western Blot. SOD1 knockdown was achieved with siRNA or miRNA mimic transfection. MicroRNA specificity was determined by 3'UTR reporter assay. Oral LQB-118 treatment (10 mg/kg/day) efficacy was determined in athymic male nude mice bearing subcutaneous PC3 xenograft tumors. RESULTS: LQB-118 treatment triggered PCa cell death and apoptosis. Therapeutic activity was at least partially dependent upon quinone reduction and ROS generation. LQB-118 treatment caused an increase in cellular ROS and lipid peroxidation. Treated cells exhibited elevated levels of NQO1, Nrf2, and SOD1. The miRNAs miR-206, miR-1, and miR-101 targeted and reduced SOD1 expression. The knockdown of SOD1, by siRNA or miRNA, enhanced LQB-118 cytotoxicity. Orally administered LQB-118 treatment significantly reduced the growth of established PCa xenograft tumors. CONCLUSION: LQB-118 is a developing and orally active pterocarpanquinone agent that effectively kills PCa cells through quinone reduction and ROS generation. The inhibition SOD1 expression enhances LQB-118 activity, presumably by impairing the cellular antioxidant response.

Photobiomodulation prevents DNA fragmentation of alveolar epithelial cells and alters the mRNA levels of caspase 3 and Bcl-2 genes in acute lung injury.

Acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are defined as pulmonary inflammation that could occur from sepsis and lead to pulmonary permeability and alveolar edema making them life-threatening diseases. Photobiomodulation (PBM) properties have been widely described in the literature in several inflammatory diseases; although the mechanisms of action are not always clear, this could be a possible treatment for ARDS/ALI. Thus, the aim of this study was to evaluate the mRNA levels from caspase-3 and BCL-2 genes and DNA fragmentation in lung tissue from Wistar rats affected by ALI and subjected to photobiomodulation by exposure to a low power infrared laser (808 nm; 100 mW; 3.571 W cm-2; four points per lung). Adult male Wistar rats were randomized into 6 groups (n = 5, for each group): control, PBM10 (10 J cm-2, 2 J and 2 seconds), PBM20 (20 J cm-2, 5 J and 5 seconds), ALI, ALI + PBM10 and ALI + PBM20. ALI was induced by intraperitoneal Escherichia coli lipopolysaccharide injection. Lung samples were collected and divided for mRNA expression of caspase-3 and Bcl-2 and DNA fragmentation quantifications. Data show that caspase-3 mRNA levels are reduced and Bcl-2 mRNA levels increased in ALI after low power infrared laser exposure when compared to the non-exposed ALI group. DNA fragmentation increased in inflammatory infiltrate cells and reduced in alveolar cells. Our research shows that photobiomodulation can alter relative mRNA levels in genes involved in the apoptotic process and DNA fragmentation in inflammatory and alveolar cells after lipopolysaccharide-induced acute lung injury. Also, inflammatory cell apoptosis is part of the photobiomodulation effects induced by exposure to a low power infrared laser.

Emphysema induced by elastase alters the mRNA relative levels from DNA repair genes in acute lung injury in response to sepsis induced by lipopolysaccharide administration in Wistar rats.

Purpose/Aim of the study: Patients suffering from chronic obstructive pulmonary disease (COPD) in association with acute respiratory distress syndrome (ARDS) present oxidative stress in lung cells, with production of free radicals and DNA lesions in pulmonary and adjacent cells. Once the DNA molecule is damaged, a set of enzymatic mechanisms are trigged to preserve genetic code integrity and cellular homeostasis. These enzymatic mechanisms include the base and the nucleotide excision repair pathways, as well as telomere regulation. Thus, the aim of this work was to evaluate the mRNA levels from APEX1, ERCC2, TP53, and TRF2 genes in lung tissue from Wistar rats affected by acute lung injury in response to sepsis and emphysema. MATERIALS AND METHODS: Adult male Wistar rats were randomized into 4 groups (n = 6, for each group): control, emphysema, sepsis, and emphysema with sepsis. Pulmonary emphysema was induced by intratracheal instillation of elastase (12 IU/animal) and sepsis induced by intraperitoneal Escherichia coli lipopolysaccharide (LPS) injection (10 mg/kg). Lungs were removed, and samples were withdrawn for histological analysis and total RNA extraction, cDNA synthesis, and mRNA level evaluation by real time quantitative polymerase chain reaction. RESULTS: Data show acute lung injury by LPS and emphysema by elastase and that APEX1, ERCC2, TP53, and TRF2 mRNA levels are increased significantly (p < 0.01) in emphysema with sepsis group. CONCLUSION: Our results suggest that alteration in mRNA levels from DNA repair and genomic stability could be part of cell response to acute lung injury in response to emphysema and sepsis.

Photobiomodulation effects on mRNA levels from genomic and chromosome stabilization genes in injured muscle.

Muscle injuries are the most prevalent type of injury in sports. A great number of athletes have relapsed in muscle injuries not being treated properly. Photobiomodulation therapy is an inexpensive and safe technique with many benefits in muscle injury treatment. However, little has been explored about the infrared laser effects on DNA and telomeres in muscle injuries. Thus, the aim of this study was to evaluate photobiomodulation effects on mRNA relative levels from genes related to telomere and genomic stabilization in injured muscle. Wistar male rats were randomly divided into six groups: control, laser 25 mW, laser 75 mW, injury, injury laser 25 mW, and injury laser 75 mW. Photobiomodulation was performed with 904 nm, 3 J/cm2 at 25 or 75 mW. Cryoinjury was induced by two applications of a metal probe cooled in liquid nitrogen directly on the tibialis anterior muscle. After euthanasia, skeletal muscle samples were withdrawn and total RNA extracted for evaluation of mRNA levels from genomic (ATM and p53) and chromosome stabilization (TRF1 and TRF2) genes by real-time quantitative polymerization chain reaction. Data show that photobiomodulation reduces the mRNA levels from ATM and p53, as well reduces mRNA levels from TRF1 and TRF2 at 25 and 75 mW in injured skeletal muscle. In conclusion, photobiomodulation alters mRNA relative levels from genes related to genomic and telomere stabilization in injured skeletal muscle.