This data article reports tissue iron, copper and zinc and liver gene expression in wild-type and parkin knockout mice given oral manganese at 0, 11 or 25 mg/kg per day from birth to day 28. Liver iron fell with manganese dose in both strains, and liver manganese and iron were inversely related. Liver expression of the iron regulator hepcidin and of the manganese and iron exporters tracked liver iron.
Key numbers
- Wild-type liver iron: 116.0 ± 11.6 µg/g at 0 mg/kg-day, 91.6 ± 9.66 at 11 and 56.1 ± 5.36 at 25 mg/kg-day (mean ± SEM; n = 10 to 11) (Table 1, p. 910).
- Parkin mouse liver iron: 99.4 ± 12.6, 68.0 ± 6.24 and 59.9 ± 4.66 µg/g at 0, 11 and 25 mg/kg-day (Table 1).
- Wild-type liver gene expression at 25 mg/kg-day (% of control): hepcidin (Hamp) 25.7 ± 6.5; Slc30a10 42.3 ± 5.7; Slc40a1 71.3 ± 11.8 (Table 2, p. 912).
- Basal diet contained 10 ppm manganese and 35 ppm iron (Methods, p. 912).
Methods (brief)
Pups received aqueous manganese chloride by mouth with a micropipette daily from postnatal day 1 to 28 and were necropsied on day 29. Tissues were acid digested and analyzed for metals by spectroscopy; liver gene expression was measured by quantitative PCR. A companion paper reports the primary behavioral findings.
Evidence fitness
The data support an animal-level statement that high early-life oral manganese lowers liver iron and alters iron-regulatory gene expression. They do not provide human dose-response information.
Limitations
The authors describe the sample size as small. High doses were used. The tissue concentration basis (wet or dry weight) is not stated in this data article.
Related evidence
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