| 包装 | 价格(元) |
| 50mg | 电议 |
| 100mg | 电议 |
| 250mg | 电议 |
| 500mg | 电议 |
Cell lines | Tobacco suspension cells |
Preparation Method | Tobacco suspension cells were treated with 100 μM fusaric acid and then analyzed for H2O2 accumulation and mitochondrial functions. |
Reaction Conditions | 100 μM; 240 min |
Applications | Cells undergoing fusaric acid-induced programmed cell death exhibited H2O2 production, lipid peroxidation, and a decrease of the catalase and ascorbate peroxidase activities. |
Animal models | crossbred barrows |
Preparation Method | A total of 40 crossbred barrows (initial weight 10 kg) were orally dosed with 0 or 200 mg of fusaric acid/kg of BW and five animals from each treatment were killed 4.5, 9, 18, or 36 h after dosing. Animals in the group killed 36 h after dosing were observed for behavioral changes. |
Dosage form | 0 or 200 mg/kg; orally |
Applications | Vomiting was noted in 60% of the pigs dosed with fusaric acid.The major neurochemical changes due to exposure to fusaric acid were seen in the hypothalamus 18 h after dosing.Brain tryptophan, serotonin, and 5-hydroxyindoleacetic acid all tended to be elevated by the action of fusaric acid. |
| 产品描述 | Fusaric acid, as a mycotoxin produced by the Fusarium species, has diverse toxicological effects in plants and animals.[1] In vitro, treatment with 104 μg/ml fusaric acid in human hepatocellular carcinoma (HepG2) cells post-translationally activates p53 in response to DNA damage.[2]In vitro efficacy test it shown that in HepG2 cells fusaric acid remarkably increased p53 promoter methylation in the 25, 104, and 150 μg/ml fusaric acid treatments; but in the 50 μg/ml fusaric acid treatment significantly decreased the promoter methylation of p53.[1]In HepG2 cells, fusaric acid dramatically increased promoter methylation of DNMT1 compared to the control; however, treatment with 25, 50, and 104 μg/ml fusaric acid decreased the promoter methylation of DNMT3A and treatment with 150 μg/ml increased the promoter methylation of DNMT3A.[3]Fusaric acid has toxicity (24 h incubation; IC50= 104 μg/ml) on mitochondrial output, cellular and mitochondrial stress responses, mitochondrial biogenesis and markers of cell death.[4]In addition, fusaric acid has cytotoxicity to PBMCs with IC50of 240.8 μg/ml and Thp-1 with IC50of 107.7 μg/ml cells at 24 h.[5] In vivo experiment it indicated that treatment with 100 mg/kg body weight fusaric acid intraperitoneally 30 min prior to the onset of the dark phase (lights out) in rats increased the level of brain serotonin (5HT), 5-hydroxyindoleacetic acid (5HIAA), tyrosine (TYRO), and dopamine (DA) and decreased the level of norepinephrine (NEpi).[6] References: |
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