富兰通过DNA损伤和莱迪格细胞的细胞亡促进细胞毒性作用
Buse Yilmaz1, Yasemin Aydin2, Banu Orta-Yilmaz2
1Department of Biology, Institute of Graduate Studies in Science and Engineering, Istanbul University, Istanbul, Turkey.
Toxicology mechanisms and methods
|July 25, 2023
概括
暴露会导致男性莱迪格细胞的DNA损伤和细胞死亡,这表明基因毒性. 这项研究研究了 furan.
科学领域:
- 毒理学 毒理学 毒理学
- 分子生物学分子生物学
- 生殖生物学 生殖生物学
背景情况:
- 是一种食物污染物,在热处理过程中形成.
- 暴露与器官毒性有关,但其基因毒性影响仍在争论中.
- furan 对男性生殖系统的基因毒性影响尚未研究.
研究的目的:
- 为了研究 furan 对 TM3 Leydig 细胞的基因毒性作用.
- 为了评估 furan 诱导的细胞毒性和男性生殖细胞中的 DNA 损伤.
主要方法:
- TM3莱迪格细胞被暴露在不同度的 (7503000μM) 中24小时.
- 细胞毒性通过细胞活力测定和乳酸脱酶 (LDH) 活性进行测量.
- 基因毒性使用亡试验,微核,彗星和染色体异常试验进行了评估.
主要成果:
- 富兰暴露显著降低了细胞活力,增加了LDH水平.
- 观察到亡的增加,结构性染色体异常,彗星形成和微核.
- 富兰在莱迪格细胞中显示出显著的基因毒性和诱导DNA损伤.
结论:
- 素在TM3 Leydig细胞中诱导显著的DNA损伤和基因毒性.
- 这些发现凸显了暴露于的潜在生殖毒性.
- 进一步的研究是有必要的,以了解 furan 的生殖健康风险.
相关概念视频
Abnormal Proliferation
4.6K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.6K
Necrosis
4.6K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
4.6K
The Intrinsic Apoptotic Pathway
6.6K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.6K


