Gupta A, Shukla G S
Neurotoxicology Research Group, Industrial Toxicology Research Centre, Lucknow, India.
J Appl Toxicol. 1996 May-Jun;16(3):227-33. doi: 10.1002/(SICI)1099-1263(199605)16:3<227::AID-JAT337>3.0.CO;2-5.
Uniparous female rats were exposed to 10 ppm cadmium (as Cd(CH3COO)2) in drinking water, ad libitum, from day 0 of pregnancy; neonates exposed to Cd gestationally and lactationally were separated from their mothers at 21 days of age and were given 10 ppm Cd in drinking water up to 45 days of age. The sequential analysis of brain lipids during development showed a significant reduction in the total lipid levels at 15, 21, 30 and 45 days of age compared to the respective controls. No change in the triglyceride levels was observed in the Cd-exposed group, except for a slight but statistically significant increase (12%, p < 0.05) at day 15 of postnatal life. Metallic exposure also decreased the cholesterol content of brain at different time intervals in comparison to its levels in age-matched control rats. The analysis of sialic acid content of the total gangliosides revealed elevated levels of this group of glycolipids at 21 (25%), 30 (17%) and 45 (23%) days of age compared to their counterpart controls. However, a remarkable reduction in the concentration of brain galactosylceramide (30-43%) and 3'-sulphogalactosylceramide (24-37%) at 21, 30 and 45 days of age was observed following pre- and postnatal exposure of cadmium in comparison to the respective controls. The ontogenic profile of different brain phospholipids in the Cd-exposed group showed an increase in the levels of phosphatidylethanolamine at 21 (31%), 30 (25%) and 45 (19%) days of age; the phosphatidylcholine contents increased at day 21 (14%), followed by a significant decrease at 30 (14%) and 45 (19%) days compared to age-matched controls. Brain phosphatidylinositol, phosphatidylserine and sphingomyelin did not show any alteration at early periods of exposure but decreased significantly following continued exposure by 34%, 45% and 21%, respectively, at 45 days of age. Metal analysis in the brain showed a reduction in zinc and copper levels at 15 and 21 days of age in Cd-exposed animals; however, iron levels remained comparable with control values throughout the experiment. It may be concluded that an early exposure of Cd may produce alteration in the development of different lipids, which may produce CNS dysfunctions with a possibility of being manifested even in later life.
从怀孕第0天起，将单胎雌性大鼠随意暴露于饮用水中10 ppm的镉（以Cd(CH3COO)2形式）；在孕期和哺乳期接触镉的新生大鼠在21日龄时与母亲分开，并在45日龄前给予饮用水中10 ppm的镉。发育过程中脑脂质的序列分析显示，与各自的对照组相比，在15、21、30和45日龄时总脂质水平显著降低。在接触镉的组中，除了出生后第15天甘油三酯水平略有但具有统计学意义的增加（12%，p < 0.05）外，未观察到甘油三酯水平的变化。与年龄匹配的对照大鼠相比，金属暴露在不同时间间隔也降低了脑胆固醇含量。对总神经节苷脂唾液酸含量的分析显示，与相应对照组相比，在21日龄（25%）、30日龄（17%）和45日龄（23%）时，这组糖脂水平升高。然而，与各自的对照组相比，在出生前和出生后接触镉后，在21、30和45日龄时观察到脑半乳糖基神经酰胺（30 - 43%）和3'-硫酸半乳糖基神经酰胺（24 - 37%）浓度显著降低。接触镉组不同脑磷脂的个体发育谱显示，在21日龄（31%）、30日龄（25%）和45日龄（19%）时磷脂酰乙醇胺水平升高；与年龄匹配的对照组相比，磷脂酰胆碱含量在21日龄时增加（14%），随后在30日龄（14%）和45日龄（19%）时显著降低。脑磷脂酰肌醇、磷脂酰丝氨酸和鞘磷脂在暴露早期未显示任何改变，但在持续暴露后，在45日龄时分别显著降低34%、45%和21%。脑中的金属分析显示，接触镉的动物在15和21日龄时锌和铜水平降低；然而，在整个实验过程中铁水平与对照值相当。可以得出结论，早期接触镉可能会导致不同脂质发育的改变，这可能会导致中枢神经系统功能障碍，甚至在以后的生活中也有可能表现出来。
