Ref ID : 6860
Caroline J. Langdon, Trevor G. Piearce, Andrew A. Meharg, and Kirk T. Semple; Inherited Resistance to Arsenate Toxicity in Two populations of Lumbricus rubellus. Environmental Toxicology & Chemistry 22(10):2344-2348, 2003
1511-1516, 2001
Reprint
In File
Notes
No unequivocal evidence exists of genetically inherited resistance to metals/metalloids in field populations of earthworms. We studied cocoon production in adult Lumbricus rubellus Hoffmeister collected from an abandoned arsenic and copper mine (Devon Great Consols, Devon, UK), and abandoned tungsten mine (Carrock Fell, Cumbria, UK) and an uncontaminated cultured population. The earthworms were kept in uncontaminated soil for nine weeks. From a total of 42 L. rubellus from each site, Devon Great Consols adults produced 301 cocoons, of which 42 were viable; Carrock Fell 60 cocoons, of which 11 were viable; and the reference population 101 cocoons, of which 62 were viable. The hatchlings were collected and stored at 4 degrees C at weekly intervals. After 12 weeks, all hatchlings were transferred to clean soil and maintained at 15 degees C for 20 weeks until they showed evidence of a clitellum. In toxicity trials, F1 generation L. rubellus were exposed to 2,000 mgAs/kg as sodium arsenate or 300 mgCu/kg as copper chloride for 28 days. The F1 generation L. rubellus from Devon Great Consols mine demonstrated resistance to arsenate but not copper. All L. rubellus from Devon Great Consols kept in soil treated with sodium arsenate remained in good condition over the 28-day period but lost condition rapidly and suffered high mortality in soil treated with copper chloride. The control population suffered high mortality in soil treated with sodium arsenate and copper chloride. Previous work has shown that field-collected adults demonstrate resistance to both arsenate and Cu toxicity under these conditions. Thus, while arsenate resistance may be demonstrated in F1 generation L. rubellus from one of the contaminated sites, Cu resistance is not. The F1 adults and F2 cocoons did not have significantly higher levels of As than the control population, with no residual As tissue burden, suggesting that resistance to As in these population may be inherited.