The genes most upregulated
by acute exposure included several metallothioneins.
Downregulated genes included the monooxygenase
CYP3A7, involved in drug and lipid metabolism.
In contrast, CYP3A7 was upregulated by chronic Cd exposure,
as was DNAJB9, an anti-apoptotic J protein.
Genes downregulated following chronic exposure included the transcriptional
regulator early growth response protein 1.
Ingenuity Pathway Analysis revealed that the top networks
altered by acute exposure were lipid metabolism, small molecule biosynthesis, cell morphology, organization,
and development;while top networks altered by chronic exposur ewere organ morphology, cell cycle, cell signaling,
and renal and urological diseases/cancer.
Many of the dysregulated genes play important roles in cellular
growth, proliferation, and apoptosis, and may be involved in carcinogenesis.
In addition to gene expression
changes, HepG2 cells treatedwith cadmium for 24 h indicated a reduction in global levels of histone methylation
and acetylation that persisted 72 h post-treatment.
The genes most upregulatedby acute exposure included several metallothioneins. Downregulated genes included the monooxygenaseCYP3A7, involved in drug and lipid metabolism. In contrast, CYP3A7 was upregulated by chronic Cd exposure,as was DNAJB9, an anti-apoptotic J protein. Genes downregulated following chronic exposure included the transcriptionalregulator early growth response protein 1. Ingenuity Pathway Analysis revealed that the top networksaltered by acute exposure were lipid metabolism, small molecule biosynthesis, cell morphology, organization,and development;while top networks altered by chronic exposur ewere organ morphology, cell cycle, cell signaling,and renal and urological diseases/cancer.Many of the dysregulated genes play important roles in cellulargrowth, proliferation, and apoptosis, and may be involved in carcinogenesis. In addition to gene expressionchanges, HepG2 cells treatedwith cadmium for 24 h indicated a reduction in global levels of histone methylationand acetylation that persisted 72 h post-treatment.
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