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Protective effects of tadalafil and N-acetyl cysteine therapy on cisplatin-induced testicular toxicity.
Int Urol Nephrol
December 2024
Department of Urology, Ankara Etlik City Hospital, Ankara, Turkey.
Purpose: To investigate whether tadalafil (TAD) and N-acetyl cysteine (NAC) can prevent cisplatin (CIS)-induced testicular toxicity.
Methods: Forty Wistar-Albino rats were divided into five groups: Control group, CIS group, TAD group, NAC group and TAD + NAC group. All groups were compared regarding body and testicular weights, testicular volumes, blood testosterone levels, testicular tissue malondialdehyde (MDA) levels, histopathological features, and testicular Cosentino and Johnsen scores.
Blue Light-Induced Mitochondrial Oxidative Damage Underlay Retinal Pigment Epithelial Cell Apoptosis.
Int J Mol Sci
November 2024
Cancer Research Program, Research Institute of the McGill University Health Centre, Montreal, QC H4A 3J1, Canada.
Reactive oxygen species (ROS) play a pivotal role in apoptosis. We reported that Blue Light (BL) induced oxidative stress in human retinal pigment epithelial (RPE) cells in vitro and increased drusen deposition and RPE cell apoptosis in human eyes. Here, we investigated the mechanisms underlying BL-induced damage to RPE cells.
View Article and Find Full Text PDFAssociation between mitophagy and inflammasome in uric acid nephropathy.
Ren Fail
December 2024
Department of Nephrology, Nantong Hospital to Nanjing University of Chinese Medicine, Nantong Hospital of Traditional Chinese Medicine, Nantong, Jiangsu, China.
Objective: This study was recruited to investigate the role of mitophagy in activating NLRP3 inflammasome in the kidney of uric acid (UA) nephropathy (UAN) rats.
Methods: This study developed a uric acid nephropathy (UAN) rat model divided into five groups: Negative control (NC), UAN model (M), UAN + autophagy inhibitor (3-MA), UAN + lysosome inhibitor (CQ), and ROS scavenger (N-acetylcysteine, N). H&E staining assessed renal structure, ROS levels were measured with 2, 7dichlorofluorescin diacetate, and ELISA measured serum markers (, , cystatin , , , ).
Mitochondrial CLPB is a pro-survival factor at the onset of granulocytic differentiation of mouse myeloblastic cells.
Apoptosis
December 2024
Department of Biochemistry and Molecular Biophysics, Kansas State University, 141 Chalmers Hall, Manhattan, KS, 66506, USA.
Article Synopsis
- Loss-of-function mutations in the CLPB gene result in congenital neutropenia, impairing the differentiation of neutrophil precursor cells, though the underlying mechanism is unclear.
- In experiments using IL-3-dependent mouse myeloblastic 32Dcl3 cells, researchers found that CLPB knockout led to decreased mitochondrial membrane potential and increased HAX1 aggregates, but did not affect cell proliferation under IL-3.
- The increased apoptosis of CLPB-deficient cells after IL-3 withdrawal was linked to reactive oxygen species (ROS), with citrate supplementation showing potential to protect these cells by enhancing ROS detoxification through ATP-citrate lyase (ACLY) activity.
The role of FOXM1 in acetylcysteine improving diabetic periodontitis.
J Mol Histol
December 2024
State Key Laboratory of Oral Diseases and National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, No. 14 3rd Section, South Renmin Road, Chengdu, Sichuan, 610041, China.
Diabetic periodontitis (DP) stems from hyperglycemia-driven oxidative stress amplification and chronic inflammation, leading to periodontal tissue breakdown. Misregulated forkhead box protein M1 (FOXM1) play key roles in this process, exacerbating both inflammation and oxidative stress. In light of N-Acetylcysteine (NAC)'s potent anti-oxidative capacity and anti-inflammatory potential, understanding how it modulates these central pathways to alleviate DP holds high scientific and clinical importance.
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