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.

Co-exposure subacute toxicity of silica nanoparticles and lead acetate on cardiovascular system

“…Recent studies have provided adequate evidence regarding cardiovascular toxicity as a result of exposure to the single pollutants like SiNPs or Pb. 20,21 The complex mixtures could have interactive effect on the catalytic levels and transcriptional proteins. 22 Our previous studies have shown adverse toxicity after co-exposure, cardiovascular toxicity in particular.…”

Effect of Lead on Human Middle Ear Epithelial Cells

“…Although lead toxicity does not occur through a single unifying mechanism, its ability to substitute for Ca 2+ is a common factor in its toxicity [10]. Lead has been reported to induce activation of several cellular and molecular processes, such as apoptosis in cancer cell models and rats [11, 12]. …”

Assessment of metals induced histopathological and gene expression changes in different organs of non-diabetic and diabetic rats

“…Different groups reported the assessment of cardiovascular damage induced by heavy metal exposure using H & E staining 35,36 . Cobbina and colleagues reported high toxicity as a result of co-exposure of metals in comparison with the individual metal exposure 37 .…”

“…Importantly, Pb and metal mixture treatment resulted in increased cardiac cell apoptosis. Previously, Xu and colleagues reported that Pb induces apoptosis in vascular and cardiac tissues 35 .…”