AI Article Synopsis
- The study investigates the impact of formalin on mouse fertility, focusing on two key apoptosis-related genes, Bcl-2 and Bax.
- Mice were divided into three groups: a control group, a group treated with formalin only, and a group treated with both formalin and L-carnitine.
- Results showed that formalin increased Bax expression and decreased Bcl-2 expression, while L-carnitine reversed these effects, suggesting it could help protect against apoptosis induced by formalin exposure.
Article Abstract
Objective: The genes Bcl-2 and Bax play important roles in apoptosis. Many studies have shown that formalin has a strong deleterious effect on male fertility and can induce apoptosis. L-carnitine has been reported to potentially reverse the negative effects of formalin, leading to improved spermatogenesis. In this study, we examined the levels of expression of Bcl-2 and Bax in mice treated with formalin and L-carnitine.
Methods: Thirty adult BALB/c mice were categorized into three groups. The mice in the control group (n=10) were not injected with any substance. The mice in the second group (n=10) received 10 mg/kg of formalin daily via an intraperitoneal injection, while those in the final group (n=10) were intraperitoneally injected daily with a dose of 10 mg/kg of formalin and 100 mg/kg of L-carnitine. All mice were kept in isolated cages for 31 days.
Results: The expression of Bax was significantly higher in the formalin-treated mice than in the mice of the control group, while the expression of Bcl-2 was significantly lower in the formalin-treated mice than in the control mice. Additionally, relative to control mice, Bcl-2 expression increased and Bax expression decreased in the mice administered both formalin and L-carnitine.
Conclusion: In this study, L-carnitine was shown to augment Bcl-2 expression and to reduce Bax expression, indicating that this compound may inhibit apoptosis. Due to its positive effects, L-carnitine can be used as a prophylactic treatment for people who routinely come into direct contact with formalin as an occupational hazard.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7482949 | PMC |
| http://dx.doi.org/10.5653/cerm.2019.03440 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Fucoxanthin alleviates the cytotoxic effects of cadmium and lead on a human osteoblast cell line.
Toxicol Res (Camb)
December 2024
Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah 21589, Saudi Arabia.
Objective: Cadmium (Cd) and lead (Pb) are non-biodegradable heavy metals (HMs) that persistently contaminate ecosystems and accumulate in bones, where they exert harmful effects. This study aimed to investigate the protective effect of fucoxanthin (FX) against the chemical toxicity induced by Cd and Pb in human bone osteoblasts in vitro, using various biochemical and molecular assays.
Methods: The effect of metals and FX on osteoblasts viability was assayed by MTT, then the effect of Pb, Cd, and FX on the cells' mitochondrial parameters was studied via assays for ATP, mitochondrial membrane potential (MMP), mitochondrial complexes, and lactate production.
Mechanistic Insights on Cardioprotective Properties of Ursolic Acid: Regulation of Mitochondrial and Non-mitochondrial Pathways.
Curr Pharm Des
December 2024
Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran.
Ursolic acid, a natural pentacyclic triterpenoid compound, has been shown to have significant cardioprotective effects in various preclinical studies. This article reviews the various mechanisms by which ursolic acid achieves its cardioprotective effects, highlighting its potent anti-oxidant, anti-inflammatory, and anti- apoptotic properties. Ursolic acid upregulates anti-oxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx), effectively reducing oxidative stress, thereby decreasing reactive oxygen species (ROS) and improving lipid peroxidation levels.
View Article and Find Full Text PDFHalcinonide activates smoothened to ameliorate ischemic stroke injury.
Life Sci
December 2024
School of Pharmacy, Lanzhou University, Lanzhou 730000, PR China; State Key Laboratory of Veterinary Etiological Biology, College of Veterinary Medicine, Lanzhou University, Lanzhou 730000, PR China; Southeast Research Institute, Lanzhou University, Lanzhou 730000, PR China. Electronic address:
Objectives: The Shh pathway may shed new light on developing new cell death inhibitors for the therapy of ischemic stroke. We aimed to examine whether the Shh co-reporter SMO or its agonist halcinonide can upregulate Bcl-2 to suppress neuronal cell death, ultimately improving behavioral deficits and reducing cerebral infarction in an ischemic stroke model.
Methods: Halcinonide or genetic manipulation of SMO was conducted in PC12 cells to examine their impacts on oxidative or OGD/R stress, and the chemical, along with AAV-SMO or AAV-EGFP were tested in MCAO rats to investigate their potential protective effects against neuronal damages due to cerebral I/R injury.
Ginsenoside Rh2 promotes cell apoptosis in T-cell acute lymphocytic leukaemia by MAPK and PI3K/AKT signalling pathways.
Nat Prod Res
December 2024
State Key Laboratory of Food Nutrition and Safety, Key Laboratory of Industrial Fermentation Microbiology, College of Biotechnology, Tianjin University of Science and Technology, Tianjin, China.
T-cell acute lymphoblastic leukaemia (T-ALL) is a common childhood malignant tumour, which has poor prognosis and high recurrence rate. Ginsenoside Rh2 (GRh2), a bioactive ingredient of has significant anti-tumour effect. In this study, we found that gene expressions of Jurkat cells were significantly changed in the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signalling pathways after 35 µm GRh2 treatment, involving in JUN, PIEN, AKT3 and MAPK8IP2.
View Article and Find Full Text PDFCircMETTL9 targets CCAR2 to induce neuronal oxidative stress and apoptosis via mitochondria-mediated pathways following traumatic brain injury.
Free Radic Biol Med
December 2024
Department of Rehabilitation Medicine, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu Province, China. Electronic address:
Traumatic brain injury (TBI) remains a principal factor in neurological disorders, often resulting in significant morbidity due to secondary neuroinflammatory and oxidative stress responses. While circular RNAs are recognized for their high expression levels in the nervous system and play crucial roles in various neurological processes, their specific contributions to the pathophysiology of TBI remain underexplored. In this study, the possible molecular mechanisms through which circMETTL9 modulated oxidative stress and neurological outcomes following TBI were investigated.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!