2008•Toxicology Mechanisms and MethodsRequires access

Studying the Effects of Lead on DNA Fragmentation and Proapoptotic Bax and Antiapoptotic Bcl-2 Protein Expression in PC12 Cells

Ali Mohammad Sharifi, Seyed Hadi Mousavi

Open publisher page 28 citations

Abstract

ABSTRACT The nervous system is one of the most important targets of lead poisoning. Despite decades of study, the exact mechanism of lead toxicity has not been fully elucidated. One of the suggested mechanisms of lead toxicity is induction of apoptosis, which has not been shown yet in some neuronal cells such as pheochromocytoma cells (PC12). Therefore, the present study sought to examine the effect of lead poisoning on apoptosis in PC12 cells as a suitable model of neuronal cell study. The present results showed that lead could induce toxicity in PC12 cells after 24 hours with as little as 1 muM in a concentration-dependent manner. In Western blot analysis, the ratio of Bax/Bcl-2 protein expression in cells incubated with 3, 30, and 90 muM lead acetate significantly increased compared to controls. Additionally, a DNA laddering pattern in lead-treated cells was shown, which could indicate nuclear fragmentation. It might be concluded that lead could cause PC12 cell death, in which apoptosis or programmed cell death plays an important role.

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ABSTRACT The nervous system is one of the most important targets of lead poisoning. Despite decades of study, the exact mechanism of lead toxicity has not been fully elucidated. One of the suggested mechanisms of lead toxicity is induction of apoptosis, which has not been shown yet in some neuronal cells such as pheochromocytoma cells (PC12). Therefore, the present study sought to examine the effect of lead poisoning on apoptosis in PC12 cells as a suitable model of neuronal cell study. The present results showed that lead could induce toxicity in PC12 cells after 24 hours with as little as 1 muM in a concentration-dependent manner. In Western blot analysis, the ratio of Bax/Bcl-2 protein expression in cells incubated with 3, 30, and 90 muM lead acetate significantly increased compared to controls. Additionally, a DNA laddering pattern in lead-treated cells was shown, which could indicate nuclear fragmentation. It might be concluded that lead could cause PC12 cell death, in which apoptosis or programmed cell death plays an important role.

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Available abstract

ABSTRACT The nervous system is one of the most important targets of lead poisoning. Despite decades of study, the exact mechanism of lead toxicity has not been fully elucidated. One of the suggested mechanisms of lead toxicity is induction of apoptosis, which has not been shown yet in some neuronal cells such as pheochromocytoma cells (PC12). Therefore, the present study sought to examine the effect of lead poisoning on apoptosis in PC12 cells as a suitable model of neuronal cell study. The present results showed that lead could induce toxicity in PC12 cells after 24 hours with as little as 1 muM in a concentration-dependent manner. In Western blot analysis, the ratio of Bax/Bcl-2 protein expression in cells incubated with 3, 30, and 90 muM lead acetate significantly increased compared to controls. Additionally, a DNA laddering pattern in lead-treated cells was shown, which could indicate nuclear fragmentation. It might be concluded that lead could cause PC12 cell death, in which apoptosis or programmed cell death plays an important role.

Key concepts: DNA laddering, Apoptosis, DNA fragmentation, Lead acetate, Programmed cell death, Toxicity, Fragmentation (computing), Cell biology

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