来自被田草污染的草地的保存饲料(Jacobaeavulgaris,Gaertn.)可能会使牲畜接触吡咯烷基生物碱(PA)。奶牛被认为是非常易感的动物,摄入PA会导致肝脏和进一步的器官损伤甚至死亡。由于缺乏数据,本研究旨在根据器官效应评估PA的临界剂量,特别关注肝脏病变和能量代谢指标。因此,将16头奶牛(每组n=4)暴露于增加的PA剂量(组:CONMoltays:<0.001mgPA/kg体重(BW)/天(d);PA1:0.47mgPA/kgBW/d;PA2:0.95mgPA/kgBW/d;PA3:1.91mgPA/kgBW/d)28天。通过每天一次口服施用定义的PA提取物来确保恒定给药。肝脏的组织学检查显示免疫细胞浸润,最高暴露组的凋亡细胞比例较高,肝细胞核增大。此外,胆汁体积随着PA剂量的增加而增加,这可能表明胆汁淤积。尽管有早期肝损伤的迹象,肝脏脂质含量和与能量代谢相关的临床化学参数,如葡萄糖,非酯化脂肪酸和β羟基丁酸,未受影响。脂肪库质量也没有随着时间的推移而显著改变,这表明PA暴露不会诱发消耗综合征。在0.95mgPA/kgBW/d的剂量下,肝脏已经显示出轻微的微观变化。然而,能量状态的短期代谢指标,脂解和酮生成,葡萄糖,NEFA和BHB,以及脂肪仓库的变化,作为脂解的长期指标,在所选方案中,所有治疗组均未受影响。这些发现表明,尽管PA相关肝细胞病变的组织病理学和临床化学证据,肝功能未受损.
Preserved feed from meadows contaminated with ragwort (Jacobaea vulgaris, Gaertn.) may expose livestock to pyrrolizidine alkaloids (PA). Dairy cows are considered to be very susceptible animals and a PA ingestion can lead to liver and further organ damages and even death. Due to the lack of data, the present study aimed to evaluate critical PA doses based on organ effects, with a special focus on liver lesions and on indicators of energy metabolism. Therefore, 16 dairy cows (n = 4 per group) were exposed to increasing PA doses (group: CONMolasses: <0.001 mg PA/kg body weight (BW)/day (d); PA1: 0.47 mg PA/kg BW/d; PA2: 0.95 mg PA/kg BW/d; PA3: 1.91 mg PA/kg BW/d) for 28 days. Constant dosing was ensured by a defined PA extract administered orally once daily. Histological examinations of the livers showed infiltration by immune cells, higher proportions of apoptotic cells and enlargement of hepatocyte nuclei in the highest exposed group. In addition, bile volume increased with PA dose, which may indicate a cholestasis. Despite the signs of incipient liver damage, liver lipid content and clinical chemical parameters related to energy metabolism, such as glucose, non-esterified fatty acids and βhydroxybutyrate, remained unaffected. Fat depot masses were also not significantly altered over time, suggesting that PA exposure did not induce a wasting syndrome. The liver showed slight microscopic changes already at a dosage of 0.95 mg PA/kg BW/d. However, the short-term metabolic indicators of energy status, lipolysis and ketogenesis, glucose, NEFA and BHB, as well as changes in fat depot, which serves as a longer-term indicator of lipolysis, remained unaffected in all treatment groups in the chosen scenario. These findings suggest that despite histopathological and clinical-chemical evidence of PA-associated hepatocellular lesions, liver function was not compromised.