塞列诺氨酸对子丸损伤的保护作用是由阿弗拉托克素B1引起的
Zhikai Zhang1, Ziqiang Zhang1, Shiyang Liu1
1College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China.
The Science of the total environment
|March 28, 2024
概括
甲 (SeMet) 通过减少氧化应激和炎症,减轻子中阿弗拉托克素B1 (AFB1) 诱导的丸损伤. 通过抑制p38/MSK/NF-κB信号通路,SeMet有效地恢复生殖健康.
科学领域:
- 毒理学 毒理学 毒理学
- 生殖生物学 生殖生物学
- 营养科学 营养科学
背景情况:
- 阿弗拉托克素B1 (AFB1) 是一种已知会导致严重丸损伤的真菌毒素.
- 氧化应激和炎症是AFB1诱导毒性的关键机制.
- 甲 (SeMet) 是一种具有抗氧化作用的微量元素.
研究的目的:
- 在子中研究SeMet对AFB1诱导的丸损伤的保护作用.
- 阐明潜在的分子机制,包括p38/MSK/NF-κB信号通路.
主要方法:
- 子接触到AFB1并接受不同剂量的SeMet治疗.
- 评估了血激素水平 (,LH,FSH) 和精液质量.
- 评估丸组织病理学 (HE染色),蛋白质表达 (IHC,IF,WB),氧化应激标志物和炎症因子 (ELISA).
主要成果:
- AFB1诱导的丸损伤,其特征是氧化应激,炎症,亡,细胞增殖受损,血液丸屏障 (BTB) 破坏,性激素减少和精液质量差.
- SeMet预治疗显著减轻了AFB1诱导的丸毒性,氧化应激和炎症.
- 观察到0.4mg/kg的SeMet具有最佳的保护作用,它抑制了p38/MSK/NF-κB通路.
结论:
- 在子中,SeMet有效地预防AFB1诱导的丸毒性.
- 保护机制包括抑制p38/MSK/NF-κB信号通路,减少氧化应激和炎症.
- 补充SeMet是一种潜在的策略,可以抵消阿弗拉托克辛诱导的生殖损伤.
相关概念视频
DNA Damage can Stall the Cell Cycle
8.5K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
8.5K
Allosteric Proteins-ATCase
4.8K
Binding sites linkages can regulate a protein's function. For example, enzyme activity is often regulated through a feedback mechanism where the end product of the biochemical process serves as an inhibitor.
Aspartate transcarbamoylase (ATCase) is a cytosolic enzyme that catalyzes the condensation of L-aspartate and carbamoyl phosphate to N-carbamoyl-L-aspartate. This reaction is the first step in pyrimidine biosynthesis. UTP and CTP, the end products of the pyrimidine synthesis...
Aspartate transcarbamoylase (ATCase) is a cytosolic enzyme that catalyzes the condensation of L-aspartate and carbamoyl phosphate to N-carbamoyl-L-aspartate. This reaction is the first step in pyrimidine biosynthesis. UTP and CTP, the end products of the pyrimidine synthesis...
4.8K
DNA Damage Can Stall the Cell Cycle
2.4K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
2.4K
Formation of the Platelet Plug
6.2K
The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
6.2K
Antifungal Agents
119
Amphotericin B is a broad-spectrum antifungal agent that exploits structural differences between fungal and mammalian cell membranes. Its amphipathic structure—featuring a hydrophobic polyene-lactone ring and a hydrophilic region containing mycosamine and carboxylic acid groups—enables selective binding to ergosterol, a sterol predominantly found in fungal plasma membranes. This selective interaction underlies the drug’s antifungal activity, although weak binding to...
119
Cellular Injury I: Introduction
68
Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
68


