College of Pharmacy, Kinjo Gakuin University, 2-1723 Omori, Moriyamaku, Nagoya, Aichi 463-8521, Japan; Faculty of Nutrition, Kobe Gakuin University, 518 Arise, Ikawadani-cho, Nishi-ku, Kobe, Hyogo 651-2180, Japan.
College of Pharmacy, Kinjo Gakuin University, 2-1723 Omori, Moriyamaku, Nagoya, Aichi 463-8521, Japan.
Heliyon. 2016 Jun 24;2(6):e00126. doi: 10.1016/j.heliyon.2016.e00126. eCollection 2016 Jun.
The aim of this study is to investigate whether a Ca-deficient diet has an attenuating effect on carbon tetrachloride (CCl4)-induced hepatotoxicity. Four-week-old male ddY mice were fed a Ca-deficient diet for 4 weeks as a part of the experimental protocol. While hypocalcemia was observed, there was no significant change in body weight. The CCl4-exposed hypocalcemic mice exhibited a significant decrease in alanine aminotransferase and aspartate aminotransferase activities at both 6 h and 24 h even though markers of renal function remained unchanged. Moreover, lipid peroxidation was impaired and total antioxidant power was partially recovered in the liver. Studies conducted in parallel with the biochemical analysis revealed that hepatic histopathological damage was attenuated 24 h post CCl4 injection in hypocalcemic mice fed the Ca-deficient diet. Finally, this diet impaired CCl4-induced inflammatory responses. Although upregulation of Ca concentration is a known indicator of terminal progression to cell death in the liver, these results suggest that Ca is also involved in other phases of CCl4-induced hepatotoxicity, via regulation of oxidative stress and inflammatory responses.
本研究旨在探讨缺钙饮食是否对四氯化碳（CCl4）诱导的肝毒性具有缓解作用。将 4 周龄雄性 ddY 小鼠用缺钙饮食喂养 4 周作为实验方案的一部分。尽管观察到低钙血症，但体重没有明显变化。在 CCl4 暴露下的低钙血症小鼠在 6 小时和 24 小时时丙氨酸氨基转移酶和天冬氨酸氨基转移酶的活性显著降低，尽管肾功能标志物保持不变。此外，肝脏中的脂质过氧化作用受损，总抗氧化能力部分恢复。与生化分析平行进行的研究表明，在 CCl4 注射后 24 小时，用缺钙饮食喂养的低钙血症小鼠的肝组织病理学损伤得到缓解。最后，这种饮食会损害 CCl4 诱导的炎症反应。虽然 Ca 浓度的上调是肝内细胞死亡终末进展的已知指标，但这些结果表明，Ca 还通过调节氧化应激和炎症反应参与 CCl4 诱导的肝毒性的其他阶段。
