Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2026
It's a gator tale: Alligator lung cells resist hexavalent chromium-induced DNA repair inhibition and chromosome instability.
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Williams Aggie R, Diven Sandra S, Meaza Idoia, Wise John Pierce
Аннотация
BACKGROUND: Hexavalent chromium [Cr(VI)] is an environmental pollutant that is widely distributed across several ecosystems, such as the aquatic environment, due to human activities. The American alligator (Alligator mississippiensis) is a top predator in the aquatic ecosystem that can inhale environmental contaminants, including Cr(VI), through airborne deposition, water surface exposure, and resuspended particles from contaminated sediments. Although Cr(VI) is a well-known human carcinogen, its health effects in alligators remain poorly understood.
METHODS: We exposed alligator lung cells to zinc chromate for 24 h or 120 h. Cytotoxicity was measured with a colony formation assay. Genotoxicity was measured with a chromosomal aberration assay and the neutral comet assay. To assess DNA repair activity, RAD51 and RAD51D foci were measured using immunofluorescence.
RESULTS: Our data showed Cr(VI) induced cytotoxicity and genotoxicity in alligator lung cells. DNA double strand breaks were elevated following both 24 and 120 h exposures with similar levels at both time points. The amount of chromosome damage increased following 24 h exposure but was reduced after 120 h exposure. We found in contrast to human lung cells, alligator lung cells had active DNA repair at both timepoints.
CONCLUSIONS: In this study, we evaluated the cytotoxic, genotoxic, and DNA repair response effects of particulate Cr(VI) in alligator lung cells after acute (24 h) and prolonged (120 h) exposures. These data indicate alligators have evolved protective measures against DNA damage induced by Cr at the cellular or molecular levels, which likely leads to protection against other chemical carcinogens that cause DNA double strand breaks. These findings inform chemical carcinogenesis in humans and support the use of alligators as sentinel species for monitoring the health impacts of Cr(VI) contamination in aquatic environments.
METHODS: We exposed alligator lung cells to zinc chromate for 24 h or 120 h. Cytotoxicity was measured with a colony formation assay. Genotoxicity was measured with a chromosomal aberration assay and the neutral comet assay. To assess DNA repair activity, RAD51 and RAD51D foci were measured using immunofluorescence.
RESULTS: Our data showed Cr(VI) induced cytotoxicity and genotoxicity in alligator lung cells. DNA double strand breaks were elevated following both 24 and 120 h exposures with similar levels at both time points. The amount of chromosome damage increased following 24 h exposure but was reduced after 120 h exposure. We found in contrast to human lung cells, alligator lung cells had active DNA repair at both timepoints.
CONCLUSIONS: In this study, we evaluated the cytotoxic, genotoxic, and DNA repair response effects of particulate Cr(VI) in alligator lung cells after acute (24 h) and prolonged (120 h) exposures. These data indicate alligators have evolved protective measures against DNA damage induced by Cr at the cellular or molecular levels, which likely leads to protection against other chemical carcinogens that cause DNA double strand breaks. These findings inform chemical carcinogenesis in humans and support the use of alligators as sentinel species for monitoring the health impacts of Cr(VI) contamination in aquatic environments.