The effects of pyridoxine deficiency and supplementation on hematological profiles, lymphocyte function, and hepatic cytochrome P450 in B6C3F1 mice
The effects of pyridoxine deficiency and supplementation on hematological profiles, lymphocyte function, and hepatic cytochrome P450 in B6C3F1 mice
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DOI：
10.1080/15476910903083866
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发表时间：
2009-01-01
影响因子：
3.3
通讯作者：
Ruchirawat, Mathuros
中科院分区：
文献类型：
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作者：
Tangjarukij, Chanthana;Navasumrit, Panida;Ruchirawat, Mathuros
吡哆醇是一种B-6维生素，是参与中间代谢的多种酶促反应的辅助因子。在B6 C3 F1小鼠中研究了吡哆醇缺乏和补充对血液学特征、淋巴细胞功能和肝脏CYP 1A 1和CYP 2 E1的影响，所述小鼠喂食含有0（即，吡哆醇缺乏饮食，[PD]）;或7 mg吡哆醇-HCl/kg（即，对照饮食，[CD]）持续8或13周，随后每天给予500 μ g盐酸吡哆醇（IP）持续连续2天（PD-S2和CD-S2）或3天（PD-S3和CD-S3）。结果表明，红细胞天冬氨酸氨基转移酶活性系数（EAST-AC）值，反映宿主吡哆醇的状态，PD小鼠显着高于CD小鼠，并下降到控制水平后补充。与CD小鼠相比，PD小鼠在接受规定饮食8周和13周后体重增加、平均红细胞体积（MCV）、血红蛋白（HGB）和红细胞压积（HCT）水平显著降低。此外，PD小鼠的总白色血细胞的循环水平显著较低，但8周后的红细胞数量较高（与CD小鼠相比）。补充吡哆醇3天使PD小鼠的HGB水平恢复至未补充CD对照的水平;与未补充PD的小鼠相比，PD-S3小鼠的HCT、MCV和MCH水平也有所增加，但未能达到与喂食对照饮食的小鼠相当的水平。吡哆醇缺乏的饮食也导致减少有丝分裂原刺激的T淋巴细胞增殖后，13周的喂养方案和增加肝脏CYP 1A 1活性，这是由吡哆醇补充逆转。这些研究表明，在小鼠模型中，吡哆醇缺乏可引起多种改变，在许多情况下，可通过补充来逆转。
Pyridoxine, a B-6 vitamin, is a co-factor in a variety of enzymatic reactions involved in intermediary metabolism. The effects of pyridoxine deficiency and supplementation on hematological profiles, lymphocyte function, and hepatic CYP1A1 and CYP2E1 were investigated in B6C3F1 mice fed a diet containing either 0 (i.e., pyridoxine deficient diet, [PD]); or 7 mg pyridoxine-HCl/kg (i.e., control diet, [CD]) for 8 or 13 weeks followed by administration of 500 mu g pyridoxine-HCl (IP) daily for either 2 (PD-S2 and CD-S2) or 3 (PD-S3 and CD-S3) consecutive days. Results demonstrated that erythrocyte aspartate aminotransferase activity coefficient (EAST-AC) values, which reflect host pyridoxine status, were significantly higher in PD mice than in CD mice, and dropped to control levels after supplementation. PD mice had significantly reduced weight gains, mean corpuscular volume (MCV), hemoglobin (HGB), and hematocrit (HCT) levels compared to CD mice after 8 and 13 weeks on the prescribed diet. In addition, PD mice had significantly lower circulating levels of total white blood cells, but higher red blood cell numbers after 8 weeks (compared to CD mice). Pyridoxine supplementation for 3 days restored HGB levels in PD mice to that of the unsupplemented CD controls; HCT, MCV and MCH levels were also increased in PD-S3 mice compared to their unsupplemented PD counterparts, but failed to reach comparable levels to those seen in mice fed a control diet. The pyridoxine-deficient diet also resulted in decreased mitogen stimulated T-lymphocyte proliferation after a 13-week feeding regimen and increased hepatic CYP1A1 activity that was reversed by pyridoxine supplementation. These studies demonstrate in a murine model that pyridoxine deficiency can cause multiple alterations that, in many cases, can be reversed by supplementation.