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Updated: May 3, 2026

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Establishing Primary Adult Fibroblast Cultures From Rodents
Published on: October 5, 2010
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Fibroblasts from long-lived rodent species exclude cadmium
Lubomír Dostál1, William M Kohler2, James E Penner-Hahn3
1Department of Chemistry, University of Michigan, Ann Arbor. Department of Pathology, University of Michigan, Ann Arbor.
Summary
Long-lived rodents resist toxic cadmium by slowing its uptake and altering metal balance. This cellular adaptation in metal homeostasis is key to their extended lifespan and reduced heavy metal toxicity.
Area of Science:
- Cell Biology
- Comparative Physiology
- Toxicology
Background:
- Fibroblast cell lines from long-lived species exhibit resistance to cellular stressors like cadmium (Cd).
- Understanding the mechanisms behind this resistance is crucial for aging and toxicology research.
Purpose of the Study:
- To investigate the cellular mechanisms underlying cadmium resistance in fibroblasts from rodents of varying lifespans.
- To determine if differences in metal uptake, export, or baseline concentrations correlate with longevity.
Main Methods:
- Inductively coupled plasma mass spectroscopy (ICP-MS) was used to quantify cadmium uptake rates in primary fibroblasts from 15 rodent species.
- Zinc export and baseline concentrations of redox-active metals (iron, copper) were also measured.
Main Results:
- Fibroblasts from long-lived rodent species demonstrated significantly slower rates of cadmium uptake compared to short-lived species.
- Short-lived species exported more zinc following cadmium exposure than long-lived species.
- Long-lived species exhibited lower baseline levels of iron and copper.
Conclusions:
- Rodent longevity is associated with cellular adaptations in metal homeostasis, including reduced cadmium uptake and altered zinc and redox-active metal handling.
- These adjustments in metal metabolism likely contribute to mitigating the toxic effects of heavy metals accumulated over longer lifespans.
- Evolutionary increases in lifespan in rodents appear linked to modifications in cellular heavy metal resistance mechanisms.

