Overview
BaSalamah and colleagues tested whether vitamin D3 altered renal and testicular injury in a controlled rat model of lead acetate toxicity. This is lane a4 toxicology evidence, not supplement occurrence evidence: lead acetate was deliberately administered in drinking water, and vitamin D3 was a co-treatment. The source reports exact tissue lead (Pb) concentrations and biochemical, cytokine, oxidative-stress, histology, and gene-expression endpoints while stating that vitamin D3 did not lower tissue Pb concentrations.
Key numbers
- Study design: 32 adult male Wistar rats, four groups, n = 8 per group, treated for four weeks.
- Lead exposure: lead acetate in drinking water at
1,000 mg/L. - Vitamin D3 co-treatment: intramuscular vitamin D3 at
1,000 IU/kg; 3 days/week. - Kidney Pb concentrations: negative control
0.124 ± 0.04 µg/g; lead positive control8.05 ± 3.12 µg/g; lead plus vitamin D37.12 ± 2.98 µg/g; vitamin D3-only normal animals0.094 ± 0.03 µg/g. - Testicular Pb concentrations: negative control
0.114 ± 0.03 µg/g; lead positive control5.45 ± 2.32 µg/g; lead plus vitamin D34.92 ± 2.18 µg/g; vitamin D3-only normal animals0.088 ± 0.04 µg/g. - Tissue Pb interpretation: the source states there was no significant difference between the lead-only and lead plus vitamin D3 groups in renal or testicular Pb concentrations.
- Serum renal and endocrine markers, negative control vs lead positive control vs lead plus vitamin D3: urea
37.16 ± 3.6,55.83 ± 5.7,45.80 ± 4.1 mg/dL; creatinine0.55 ± 0.1,0.78 ± 0.09,0.59 ± 0.07 mg/dL; calcium9.90 ± 0.64,8.63 ± 0.58,9.72 ± 0.48 mg/dL; 25-OH vitamin D23.05 ± 3.08,15.33 ± 4.13,20.16 ± 2.04 ng/mL; testosterone3.95 ± 0.91,2.38 ± 0.48,3.60 ± 0.61 ng/mL. - Serum cytokines, negative control vs lead positive control vs lead plus vitamin D3: TNF-alpha
25.01 ± 3.73,37.33 ± 7.14,27.51 ± 4.81 pg/mL; IL-47.83 ± 1.60,15.66 ± 2.33,11.16 ± 2.04 pg/mL; IL-1012.66 ± 2.22,7.01 ± 1.78,10.33 ± 1.86 pg/mL. - Kidney oxidative-stress markers, negative control vs lead positive control vs lead plus vitamin D3: MDA
33.16 ± 4.75,45.10 ± 4.97,34.81 ± 3.85 nmol/g; GSH38.82 ± 5.31,29.65 ± 3.32,36.34 ± 4.54 mg/g; GPx3.93 ± 0.95,1.82 ± 0.70,3.52 ± 0.41 µg/mg; CAT245.8 ± 34.9,175.1 ± 17.8,222.6 ± 15.4 U/mg; SOD103.2 ± 9.8,97.66 ± 16.2,104.51 ± 10.11 U/mg. - Testis oxidative-stress markers, negative control vs lead positive control vs lead plus vitamin D3: MDA
25.16 ± 3.97,38.66 ± 5.61,32.50 ± 3.10 nmol/g; GSH24.17 ± 3.37,19.02 ± 3.78,22.16 ± 3.31 mg/g; GPx2.63 ± 0.98,1.58 ± 0.30,2.40 ± 0.48 µg/mg; CAT95.33 ± 16.9,65.50 ± 14.8,92.30 ± 9.8 U/mg; SOD12.1 ± 2.28,10.66 ± 1.96,11.33 ± 2.71 U/mg.
Methods (brief)
Lead acetate trihydrate and vitamin D3 were administered to adult male Wistar rats for four weeks. Serum urea, creatinine, calcium, 25-OH vitamin D, and total testosterone were measured using Cobas e411/Cobas Integra instrumentation; serum TNF-alpha, IL-4, IL-10, renal/testicular antioxidant markers, and MDA were measured by ELISA. Renal and testicular Pb concentrations were quantified by atomic absorption spectrophotometry using a Perkin Elmer AAnalyst 800 at 283.3 nm after tissue digestion; the paper reports Pb as total Pb, not chemical species. Histopathology used Masson’s trichrome staining and TUNEL assay; immunohistochemistry and RT-PCR assessed vitamin D pathway and inflammatory markers.
Implications
Microbiome: No microbiome endpoints.
Related evidence
Update history
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