4.5 Article

Effect of Cadmium Exposure on the Histopathology of Cerebral Cortex in Juvenile Mice

期刊

BIOLOGICAL TRACE ELEMENT RESEARCH
卷 165, 期 2, 页码 167-172

出版社

HUMANA PRESS INC
DOI: 10.1007/s12011-015-0246-2

关键词

Cadmium; Histopathology; Cerebral cortex; Neurotoxicity; Juvenile mice

资金

  1. Aid Project for Leading Young Teachers in Henan Provincial Institutions of Higher Education of China [2010GGJS-136]
  2. Science and Technology Research Important Project of Education Department Henan Province [13A230142, 13A230289]

向作者/读者索取更多资源

Cadmium, a heavy metal, is a toxic environmental and industrial pollutant. Exposure to cadmium can lead to the toxic effects in a variety of tissues, also including the brain. The present study investigated the effect of cadmium exposure on the histopathology of cerebral cortex in juvenile mice. Juvenile mice were randomly divided into control, low (1.87 mg/kg), medium (3.74 mg/kg), and high (7.48 mg/kg) dose groups. After cadmium exposure by drinking water for 10 days, the cerebral cortex was obtained for histopathology studies. The medium and high dose of cadmium, rather than low dose, could induce the histopathology alterations of cerebral cortex in a dose-dependent manner. In the high-dose group, microstructure significantly showed pia mater encephali divorcing from cerebral cortex layer, serious hyperemia of blood capillary in pia mater encephali and cerebral cortex, broadening vessel peripheral clearance, a large number of eosinophil leukocyte infiltrating around blood vessel, vacuolar degeneration in part granule cells, and obviously increasing apoptotic cells. Ultrastructure obviously displayed marginalized heterochromatin, incomplete or fused nuclear membranes, broadened perinuclear space, ambiguous mitochondria cristae, decreased synaptic cleft, and fused presynaptic and postsynaptic membrane. Our results revealed that cadmium at the middle and high dose could induce obvious microstructure and ultrastructure alterations of cerebral cortex in juvenile mice, which may be one important mechanism of cadmium neurotoxicity.

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