title: Lead Induces Apoptosis and Histone Hyperacetylation in Rat Cardiovascular Tissues.
abstract: Acute and chronic lead (Pb) exposure might cause hypertension and cardiovascular diseases. The purpose of this study was to evaluate the effects of early acute exposure to Pb on the cellular morphology, apoptosis, and proliferation in rats and to elucidate the early mechanisms involved in the development of Pb-induced hypertension. Very young Sprague-Dawley rats were allowed to drink 1% Pb acetate for 12 and 40 days. Western blot analysis indicated that the expression of proliferating cell nuclear antigen (PCNA) decreased in the tissues of the abdominal and thoracic aortas and increased in the cardiac tissue after 12 and 40 days of Pb exposure, respectively. Bax was upregulated and Bcl-2 was downregulated in vascular and cardiac tissues after 40 days of Pb exposure. In addition, an increase in caspase-3 activity was observed after 40 days of exposure to Pb. In terms of morphology, we found that the internal elastic lamina (IEL) of aorta lost the original curve and the diameter of cardiac cell was enlarged after 40 days. Furthermore, the exposure led to a marked increase in acetylated histone H3 levels in the aortas and cardiac tissue after 12 and 40 days, than that in the control group. These findings indicate that Pb might increase the level of histone acetylation and induce apoptosis in vascular and cardiac tissues. However, the mechanism involved need to be further investigated.
authors.affiliation: Department of Biochemistry and Molecular Biology, Hebei Medical University, Shijiazhuang, 050017, China.
authors.forename: Li-Hui
authors.initials: LH
authors.lastname: Xu
authors.affiliation: College of Public Health, Hebei Medical University, Shijiazhuang, 050017, China.
authors.forename: Fang-Fang
authors.initials: FF
authors.lastname: Mu
authors.affiliation: The Second Hospital, Hebei Medical University, Shijiazhuang, 050000, China.
authors.forename: Jian-Hong
authors.initials: JH
authors.lastname: Zhao
authors.affiliation: The Second Hospital, Hebei Medical University, Shijiazhuang, 050000, China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: He
authors.affiliation: Laboratory of Neurobiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang, 050017, China.
authors.forename: Cui-Li
authors.initials: CL
authors.lastname: Cao
authors.affiliation: College of Public Health, Hebei Medical University, Shijiazhuang, 050017, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Yang
authors.affiliation: College of Public Health, Hebei Medical University, Shijiazhuang, 050017, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Liu
authors.affiliation: College of Public Health, Hebei Medical University, Shijiazhuang, 050017, China.
authors.forename: Xue-Hui
authors.initials: XH
authors.lastname: Liu
authors.affiliation: College of Public Health, Hebei Medical University, Shijiazhuang, 050017, China.
authors.forename: Su-Ju
authors.initials: SJ
authors.lastname: Sun
mesh_terms: D000107:Acetylation; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects*; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism; D001794:Blood Pressure; D001808:Blood Vessels / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D053148:Caspase 3 / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D006321:Heart / Q000187:drug effects; D006657:Histones / Q000378:metabolism*; D007854:Lead / Q000097:blood / Q000378:metabolism / Q000494:pharmacology*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D051381:Rats
chemical_list: D051017:Apoptosis Regulatory Proteins; D006657:Histones; D007854:Lead; D053148:Caspase 3