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首页> 外文期刊>Journal of biochemical and molecular toxicology >Vitamin D_3 and calcium cosupplementation alleviates cadmium hepatotoxicity in the rat: Enhanced antioxidative and anti-inflammatory actions by remodeling cellular calcium pathways
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Vitamin D_3 and calcium cosupplementation alleviates cadmium hepatotoxicity in the rat: Enhanced antioxidative and anti-inflammatory actions by remodeling cellular calcium pathways

机译：维生素D_3和钙腐护减轻了大鼠肝毒性：通过重塑细胞钙途径来增强抗氧化和抗炎作用

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Although vitamin D (VD) and calcium (Ca) attenuate cadmium (Cd) metabolism, their combined antioxidant and anti-inflammatory actions against Cd toxicity have not been previously explored. Hence, this study measured the protective effects of VD ± Ca supplements against Cd hepatotoxicity. Forty adult male rats were distributed to: negative controls (NCs), positive controls (PCs), VD, Ca, and VD_3 and Ca (VDC) groups. All groups, except NC, received CdCI_2 in drinking water (44 mg/L) for 4 weeks individually or concurrently with intramuscular VD_3 (600IU/kg; three times per week) and/or oral Ca (100 mg/kg; five times per week). The PC group showed abnormal hepatic biochemical parameters and increase in cellular cytochrome C, caspase-9, and caspase-3 alongside the apoptotic/necrotic cell numbers by terminal deoxynucleotidyl transferase dUTP nick end labeling technique. The PC hepatic tissue also had substantially elevated pro-oxidants (malondialdehyde [MDA]/H_2O_2/protein carbonyls) and inflammatory cytokines (inter-leukin 1β [IL-1β]/IL-6/IL17A/tumor necrosis factor-α), whereas the anti-inflammatory (IL-10/IL-22) and antioxidants (glutathione [GSH]/GPx/catalase enzyme [CAT]) markers declined. Hypovitaminosis D, low hepatic tissue Ca, aberrant hepatic expression of VD-metabolizing enzymes (Cyp2R1/Cyp27a1/cyp24a1), receptor and binding protein alongside Ca-membrane (Cav1.1/Cav3.1), and store-operated (RyR1/ITPR1) channels, and Ca-binding proteins (CAM/CAMKIIA/S100A1/S100B) were observed in the PC group. Both monotherapies decreased serum, but not tissue Cd levels, restored the targeted hepatic VD/Ca molecules' expression. However, these effects were more prominent in the VD group than the Ca group. The VDC group, contrariwise, disclosed the greatest alleviations on serum and tissue Cd, inflammatory and oxidative markers, the VD/Ca molecules and tissue integrity. In conclusion, this report is the first to reveal boosted protection for cosupplementing VD and Ca against Cd hepatotoxicity that could be due to enhanced antioxidative, anti-inflammatory, and modulation of the Ca pathways.
机译：虽然维生素D（VD）和钙（Ca）会减弱镉（Cd）的代谢，但它们的抗氧化和抗炎联合作用对抗镉毒性之前尚未被探索过。因此，本研究测量了VD±Ca补充剂对镉肝毒性的保护作用。将40只成年雄性大鼠分为：阴性对照组（NCs）、阳性对照组（PCs）、VD、Ca、VD_3和Ca（VDC）组。除NC外，所有组均单独或同时接受饮用水中的CdCI_2（44 mg/L）治疗4周，同时接受肌肉内VD_3（600 IU/kg；每周三次）和/或口服Ca（100 mg/kg；每周五次）。通过末端脱氧核苷酸转移酶dUTP缺口末端标记技术，PC组显示异常的肝脏生化参数，细胞色素C、半胱天冬酶-9和半胱天冬酶-3以及凋亡/坏死细胞数量增加。PC肝组织中的促氧化剂（丙二醛[MDA]/过氧化氢/蛋白质羰基）和炎性细胞因子（白细胞介素1β[IL-1β]/白细胞介素6/IL 17a/肿瘤坏死因子-α）显著升高，而抗炎剂（IL-10/IL-22）和抗氧化剂（谷胱甘肽[GSH]/GPx/过氧化氢酶[CAT]）标记物则下降。PC组出现低维生素D、低肝组织钙、VD代谢酶（Cyp2R1/Cyp27a1/cyp24a1）、钙膜旁受体和结合蛋白（Cav1.1/Cav3.1）、储存操作（RyR1/ITPR1）通道和钙结合蛋白（CAM/CAMKIIA/S100A1/S100B）的异常肝表达。两种单一疗法均能降低血清（而非组织Cd）水平，恢复靶向肝脏VD/Ca分子的表达。然而，这些影响在VD组比Ca组更显著。相反，VDC组在血清和组织Cd、炎症和氧化标记物、VD/Ca分子和组织完整性方面表现出最大的缓解。总之，本报告首次揭示了协同补充VD和Ca对Cd肝毒性的增强保护作用，这可能是由于增强了抗氧化、抗炎和Ca途径的调节。

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