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Melatonin Protection against Lead-Induced Changes in Human Neuroblastoma Cell Cultures

National Institute of Nutrition, Hyderabad, India

Adanna O. Dennis
Josephine Heinz

Savannah State University, Savannah, Georgia, USA

Mohan C. Vemuri

Childrens’ Hospital of Philadelphia, Philadelphia, Pennsylvania, USA

C. S. Chetty

Savannah State University, Savannah, Georgia, USA

Correspondence: Address correspondence to Chellu S. Chetty, PhD, PO Box 20600, Savannah State University, Savannah, GA 31404, USA. E-mail:chettyc{at}savstate.edu

The nervous system is the primary target for low-levels of lead (Pb) exposure and the developing brain appears to be especially vulnerable to Pb neurotoxicity. Chronic low-level Pb exposure causes growth retardation and intellectual impairment. In the present study the protective effect of melatonin during exposure to low-levels of Pb in human SH-SY5Y neuroblastoma cell cultures was assessed. The cells were exposed to Pb (0.01 to 10 µM) for 48 h. Pb inhibited the proliferation of neuroblastoma cells significantly in a concentration-dependent manner. A 50% inhibition (IC₅₀) of cell proliferation was observed at about 5 µM Pb. Pb decreased (16% to 62%) the levels of total cellular glutathione (GSH) in a concentration (0.1 to 10 µM)-dependent manner. Exposure of cells to Pb (5 µM) for 48 h resulted in an eightfold increase in caspase-3 activity and prostaglandin E₂ (PGE₂) level. Pretreatment with melatonin (10 µM) blocked the effects of Pb on GSH content and caspase-3 activity, and showed significant improvement in reducing the level of PGE₂. The results suggest that some of the neurotoxic effects of Pb may be partly mediated by apoptosis and pretreatment with melatonin can prevent these effects. The present study asserts the neuroprotective effect of melatonin in conditions of Pb-induced toxicity in neuroblastoma cell cultures.

Key Words: Caspase-3 • Glutathione • Lead • Melatonin • Neuroblastoma Cells • Neuroprotection • Prostaglandin E₂

International Journal of Toxicology, Vol. 25, No. 6, 459-464 (2006)
DOI: 10.1080/10915810600959576


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