Aflatoxin B1, as a class of carcinogenic mycotoxins produced by Aspergillus fungi, always lead to the development of hepatocellular carcinoma (HCC) in humans and animals.[1] Aflatoxin B1's toxicity includes acute toxicity, teratogenicity, mutagenicity and carcinogenicity. Moreover, DNA adduction, inflammation and oxidative stress caused by Aflatoxin B1 can also participate in the occurrence of cancer.[2]
In vitro, AFB1 has inhibition against cell viability of Hek293 cells with IC50 of 32.60 μM.[3] In vitro experiment it shown that with 0, 10, 50, and 100 μM AFB1, maturation of oocytes was performed. At concentrations of 50 and 100 μM AFB1, the number of oocytes reaching the metaphase II stage reduced and the oocytes presented with lower intracellular levels of GSH. And intracellular ROS production in matured oocytes also reached the highest-level.[4]
In vivo test it shown that treatment with 5 mg/kg Aflatoxin B1 intraperitoneally in chicks markedly boost ALT and AST levels (indicators of liver damage).[5] In vivo efficacy test it exhibited that Aflatoxin B1 impairs animal performance following a subacute or chronic exposure, the LD50 values vary from 0.3 mg/kg body weight in ducklings to 9.0 mg/kg body weight in mice and up to 17.9 mg/kg body weight in female rats. [6] Pregnant mice were treated with a high dose of 20 mg/kg Aflatoxin B1 intraperitoneally, there has peak absorption in blood after 15 min, which was delayed to 30 min after oral ingestion, suggesting aflatoxin's uptake from the proximal intestine was very rapid. [7] In vivo, at a high-dose 75 μg/kg, Aflatoxin B1 significantly shown an over 70% reduction in the levels of fecal short-chain fatty acids (SCFAs). Moreover, Rats were treated with 25 μg/kg Aflatoxin B1 orally caused a remarkable elevations of fecal cholic acid (2.18-fold), linoleic acid (cis-9, cis-12-18:2) (11.3-fold), pentadecanoic acid (15: 0) (3.68-fold), pyruvic acid (4.56-fold), and 3-phenyllactic acid (3.74-fold).[8]
参考文献:
[1] Rushing BR, Selim MI. Aflatoxin B1: A review on metabolism, toxicity, occurrence in food, occupational exposure, and detoxification methods. Food Chem Toxicol. 2019 Feb;124:81-100.
[2] Cao W, et al. Aflatoxin B1: metabolism, toxicology, and its involvement in oxidative stress and cancer development. Toxicol Mech Methods. 2022 Jul;32(6):395-419.
[3] Dlamini NZ, et al. Toxicogenicity and mechanistic pathways of aflatoxin B1 induced renal injury. Environ Toxicol. 2021 Sep;36(9):1857-1872.
[4] Hajarizadeh A, et al. Aflatoxin B1 impairs in vitro early developmental competence of ovine oocytes. Theriogenology. 2022 Apr 15;183:53-60.
[5] Gao X, et al. Morin alleviates aflatoxin B1-induced liver and kidney injury by inhibiting heterophil extracellular traps release, oxidative stress and inflammatory responses in chicks. Poult Sci. 2021 Dec;100(12):101513.
[6] Agag B. Mycotoxins in foods and feeds: 1-aflatoxins. Ass. Univ. Bull. Environ. Res. 2004;7:173–205.
[7] Bastaki S.A., et al. Toxicokinetics of Aflatoxin in Pregnant Mice. Int. J. Toxicol. 2010;29:425–431.
[8] Zhou J, et al. Aflatoxin B1 Disrupts Gut-Microbial Metabolisms of Short-Chain Fatty Acids, Long-Chain Fatty Acids, and Bile Acids in Male F344 Rats. Toxicol Sci. 2018 Aug 1;164(2):453-464.
黄曲霉毒素B1作为一类由曲霉属真菌产生的致癌真菌毒素，常导致人和动物发生肝细胞癌。[1] 黄曲霉毒素B1的毒性包括急性毒性、致畸性、致突变性和致癌性。此外，黄曲霉毒素B1引起的DNA内加、炎症和氧化应激等也参与了癌症的发生。[2]
在体外，AFB1 对 Hek293 细胞的细胞活力具有抑制作用，IC50 为 32.60 μM。[3] 体外实验表明，在 0、10、50 和 100 μM AFB1 作用下，成熟卵母细胞进行了。在 50 和 100 μM AFB1 浓度下，达到中期 II 期的卵母细胞数量减少，并且卵母细胞细胞内 GSH 水平较低。并且成熟卵母细胞细胞内ROS的产生也达到了最高水平。[4]
体内试验表明，用 5 mg/kg 黄曲霉毒素 B1 对小鸡进行腹膜内处理可显着提高 ALT 和 AST 水平（肝损伤指标）。[5] 体内功效试验表明黄曲霉毒素 B1 在亚急性或慢性接触后会损害动物的表现，LD50 值从小鸭的 0.3 毫克/千克体重到小鼠的 9.0 毫克/千克体重和雌性大鼠的 17.9 毫克/千克体重不等。 [6] 孕鼠腹腔注射高剂量黄曲霉毒素B1 20 mg/kg，15 min后出现血液吸收峰，口服后延迟至30 min，提示黄曲霉毒素的摄取来自近端肠道的速度非常快。 [7] 在体内，在 75 μg/kg 的高剂量下，黄曲霉毒素 B1 显着降低了粪便短链脂肪酸 (SCFA) 水平 70% 以上。此外，给大鼠口服 25 μg/kg 黄曲霉毒素 B1，导致粪便胆酸（2.18 倍）、亚油酸（cis-9、cis-12-18:2）（11.3 倍）、十五烷酸显着升高(15:0)（3.68 倍）、丙酮酸（4.56 倍）和 3-苯基乳酸（3.74 倍）。[8]
| Cell experiment [1]: | |
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Cell lines |
HepG2 cells |
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Preparation Method |
Aflatoxin B1 (100 μM) was treated at 85 kV with HVACP for 0, 2, 5, 10, and 20 min. HepG2 cells were exposed to HVACP-treated Aflatoxin B1 for 72 h and assessed for cell viability, caspase-3 activity, DNA fragmentation, and protein carbonyls for each treatment time. |
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Reaction Conditions |
100 μM; 0, 2, 5, 10, and 20 min |
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Applications |
Cell viability, caspase-3 activity, DNA fragmentation levels, and protein carbonyls contents of HepG2 cells exposed to HVACP-treated Aflatoxin B1 after 20 min was not significantly different compared to non-exposed HepG2 cells. However, their contents were significantly higher in non-exposed cells compared to the other HVACP treatment times. |
| Animal experiment [2]: | |
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Animal models |
Male Wistar rats |
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Dosage form |
10, 20, or 50 μg/kg; i.m. |
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Preparation method |
Male Wistar rats were injected intramuscularly with doses of 10, 20, or 50 μg Aflatoxin B1/kg body weight on alternate days from 45 to 100 days of age. |
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Applications |
Significant reductions in body weights, relative weights of reproductive organs, daily sperm production, epididymal sperm count, viable sperm, motile sperm, and hypoosmotic swelling-tail coiled sperm were observed. Significant decreases in testicular steroidogenic enzymes and serum testosterone levels were also observed indicating decreased steroidogenesis. |
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参考文献: [1] Nishimwe K, et al. Cytotoxicity assessment of Aflatoxin B1 after high voltage atmospheric cold plasma treatment. Toxicon. 2021 Apr 30;194:17-22. |
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