These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Perturbations of intracellular calcium distribution in kidney cells by nephrotoxic haloalkenyl cysteine S-conjugates.
    Author: Vamvakas S, Sharma VK, Sheu SS, Anders MW.
    Journal: Mol Pharmacol; 1990 Oct; 38(4):455-61. PubMed ID: 2233687.
    Abstract:
    The Ca2(+)-sensitive dye fura-2 was used to investigate the disturbances in intracellular Ca2+ concentration [( Ca2+]i) and distribution induced by the nephrotoxic cysteine S-conjugate S-(1,2-dichlorovinyl)-L-cysteine (DCVC) and its homocysteine analog S-(1,2-dichlorovinyl)-L-homocysteine (DCVHC) in LLC-PK1 cells. After 24-hr treatment with DCVC, the average [Ca2+]i increased from 88 +/- 23 nM to 415 +/- 92 nM. Digital image analysis revealed that the mitochondrial region, which was stained with rhodamine-123, contained lower Ca2+ concentration ([Ca2+]) than other cell areas. This distribution was different from the higher [Ca2+] in the nuclear and mitochondrial regions observed in control cells. In DCVHC-treated cells, there was also an increase in [Ca2+]i to 355 +/- 85 nM, but the increase in [Ca2+] was greater in the mitochondrial region, compared with the rest of the cell. After 72-hr treatment with DCVC or DCVHC, the average [Ca2+]i was 410 +/- 85 nM and 340 +/- 90 nM, respectively, and blebs with markedly higher [Ca2+] (600-1000 nM) than the rest of the cell appeared in both DCVC- and DCVHC-treated cells. Moreover, in DCVC-treated cells the mitochondria could not be stained with rhodamine-123, indicating severe mitochondrial damage and loss of membrane potential. All changes described above took place in viable (propidium iodide-negative) cells. The experiments demonstrate that severe perturbations of intracellular Ca2+ distribution, particularly in the mitochondrial region, precede bleb formation and cell death in the course of development of toxicity by DCVC and DCVHC.
    [Abstract] [Full Text] [Related] [New Search]