马兜铃酸A /Aristolochic acid A {[allProObj[0].p_purity_real_show]}
货号：A714436同义名：
马兜铃酸
/ Aristolochic acid I;TR 1736
Aristolochic acid A是一种从马兜铃科植物（Aristolochia debilis Sieb. et Zucc.）中提取的天然产物，强烈引起卵巢成熟过程中通过抑制Akt磷酸化介导的凋亡抑制的毒性损伤。
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Type
HazMat fee for 500 gram (Estimated)
Excepted Quantity
USD 0.00
Limited Quantity
USD 15-60
Inaccessible (Haz class 6.1), Domestic
USD 80+
Inaccessible (Haz class 6.1), International
USD 150+
Accessible (Haz class 3, 4, 5 or 8), Domestic
USD 100+
Accessible (Haz class 3, 4, 5 or 8), International
Aristolochic Acid A (Aristolochic acid I), is the main component of plant extract Aristolochic acids, which are found in various herbal plants of genus Aristolochia and Asarum, strongly induces toxic damage during ovarian maturation by inhibiting Akt phosphorylation-mediated suppression of apoptosis. Aristolochic acid A (150, 200 μM, 24 hours) inhibits the cell viabilities of kidney cells HEK293 and HK-2. Aristolochic acid A (100, 200 μM, 24 hours) causes a concentration-dependent decrease in bladder cancer-associated protein (BLCAP) mRNA levels in kidney cells (HEK 293 and HK-2), and bladder cancer cell line (HT-1376). Aristolochic acid A (100, 200 μM, 24 hours) weakens the BLCAP protein signals in a dose-dependent manner in both HEK293 and HT-1376 cells[3]. AA (Aristolochic Acid A) has been found to damage broilers' kidneys by breaking the redox balance to form oxidative stress, along with promoting apoptosis of renal cells[4]. Additionally, AAI promoted apoptosis in SSCs, which was accompanied by upregulation of caspase 3, P53 and BAX expression and downregulation of Bcl-2 expression, and suppressed autophagy, which was accompanied by upregulation of P62 expression and downregulation of ATG5 and LC3B expression, in a concentration-dependent manner. AAI (Aristolochic acid I) impaired spermatogenesis in rats, as identified by degeneration of the seminiferous epithelium, and increased apoptosis of testicular cells[5]. The mechanism of AA-I-induced hepatotoxicity was associated with oxidative-stress-mediated apoptosis and mitochondrial damage[6].
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