Keywords: 
• lead /
• yeast cell /
• cytotoxity /
• ROS /
• Ca²⁺

Abstract: This paper was conducted to research the cellular toxicity of lead based on the model yeasts to explore the role that intracellular reactive oxygen species (ROS) and Ca²⁺ play in the mechanism of the cell death induced by lead. The results revealed that the cellular bioactivity of yeasts was inhibited by lead nitrate at the concentration from 5 to 100 mg·L^-1and the cell death induced by lead was found. Yeast cell mortality increases with the increase of lead concentration and the extension of time. The levels of ROS and Ca²⁺ elevated significantly and the mitochondrial membrane potential decreased dramatically in yeast cells under lead stress. Cell death induced by lead was decreased by ascorbic acid (AsA) at the concentration of 1 mmol·L^-1 and was inhibited by the calcium chelator (EGTA) at the concentration of 0.5 mmol·L^-1 or the specific inhibitor of plasma membrane Ca²⁺ channel (LaCl₃) at the concentration of 0.1 mmol·L^-1. The results showed that cell death induced by lead was related to the levels of intracellular ROS and Ca²⁺. The opening of mitochondrial membrane permeability transition pore channels may be induced by high levels of Ca²⁺, or mitochondrial membranes were broken by high levels of ROS, which lead to decreasing membrane potential and cause cell death by activating down-stream relevant signal pathways.