Lead is an omnipresent pollutant, and its contamination in natural waters is an issue of current regulatory concern throughout the world including Canada. The free divalent ion of lead (Pb2+) is considered to be the most bioavailable and toxic form of lead. Pb2+ is known to be a calcium antagonist in vertebrates including fish. It is believed that lead causes toxicity to freshwater fish primarily by disrupting ionic homeostasis both during acute and chronic waterborne exposure. Lead can also potentially act as a respiratory toxicant since it is known to impair hemoglobin synthesis in both vertebrates. To date, the mechanistic underpinnings of lead accumulation and toxicity in aquatic invertebrates are not well understood, particularly during acute exposure. Therefore, the main objectives of the present study were in two folds: (i) to investigate the mechanisms of waterborne lead uptake, and (ii) to understand the physiological basis of lead toxicity during acute exposure. I used freshwater crustacean, <i>Daphnia magna</i>, as a model freshwater invertebrate species for my study. <i>Daphnia</i> are known to be quite sensitive to metals and widely used as a model species for toxicity assessments. The results of my study suggest that lead inhibits waterborne Ca2+ uptake in <i>Daphnia</i> in a concentration dependent manner, and this inhibition occurs predominantly through a direct competitive interaction. The entry of waterborne Pb2+ in <i>Daphnia</i> likely occurs via both lanthanum-sensitive and verapamil-sensitive epithelial calcium channels. Moreover, my results also indicate that acute waterborne lead exposure severely disrupts both Ca2+ and Na+ uptake from water, which are concomitant with the increase in the lead body burden in <i>Daphnia</i>. Interestingly however, acute exposure to lead does not affect the rate of oxygen consumption in <i>Daphnia</i>, indicating no acute respiratory toxicity of lead. Overall, it appears that lead acts as an ionoregulatory toxicant to <i>Daphnia</i> during acute waterborne exposure.

Lead is an omnipresent pollutant, and its contamination in natural waters is an issue of current regulatory concern throughout the world including Canada. The free divalent ion of lead (Pb2+) is considered to be the most bioavailable and toxic form of lead. Pb2+ is known to be a calcium antagonist in vertebrates including fish. It is believed that lead causes toxicity to freshwater fish primarily by disrupting ionic homeostasis both during acute and chronic waterborne exposure. Lead can also potentially act as a respiratory toxicant since it is known to impair hemoglobin synthesis in both vertebrates. To date, the mechanistic underpinnings of lead accumulation and toxicity in aquatic invertebrates are not well understood, particularly during acute exposure. Therefore, the main objectives of the present study were in two folds: (i) to investigate the mechanisms of waterborne lead uptake, and (ii) to understand the physiological basis of lead toxicity during acute exposure. I used freshwater crustacean, <i>Daphnia magna</i>, as a model freshwater invertebrate species for my study. <i>Daphnia</i> are known to be quite sensitive to metals and widely used as a model species for toxicity assessments. The results of my study suggest that lead inhibits waterborne Ca2+ uptake in <i>Daphnia</i> in a concentration dependent manner, and this inhibition occurs predominantly through a direct competitive interaction. The entry of waterborne Pb2+ in <i>Daphnia</i> likely occurs via both lanthanum-sensitive and verapamil-sensitive epithelial calcium channels. Moreover, my results also indicate that acute waterborne lead exposure severely disrupts both Ca2+ and Na+ uptake from water, which are concomitant with the increase in the lead body burden in <i>Daphnia</i>. Interestingly however, acute exposure to lead does not affect the rate of oxygen consumption in <i>Daphnia</i>, indicating no acute respiratory toxicity of lead. Overall, it appears that lead acts as an ionoregulatory toxicant to <i>Daphnia</i> during acute waterborne exposure.