BaSalamah et al. 2018 - Lead acetate, vitamin D, and rat renal/testicular injury

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 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 control 8.05 ± 3.12 µg/g; lead plus vitamin D3 7.12 ± 2.98 µg/g; vitamin D3-only normal animals 0.094 ± 0.03 µg/g.
• Testicular Pb concentrations: negative control 0.114 ± 0.03 µg/g; lead positive control 5.45 ± 2.32 µg/g; lead plus vitamin D3 4.92 ± 2.18 µg/g; vitamin D3-only normal animals 0.088 ± 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; creatinine 0.55 ± 0.1, 0.78 ± 0.09, 0.59 ± 0.07 mg/dL; calcium 9.90 ± 0.64, 8.63 ± 0.58, 9.72 ± 0.48 mg/dL; 25-OH vitamin D 23.05 ± 3.08, 15.33 ± 4.13, 20.16 ± 2.04 ng/mL; testosterone 3.95 ± 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-4 7.83 ± 1.60, 15.66 ± 2.33, 11.16 ± 2.04 pg/mL; IL-10 12.66 ± 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; GSH 38.82 ± 5.31, 29.65 ± 3.32, 36.34 ± 4.54 mg/g; GPx 3.93 ± 0.95, 1.82 ± 0.70, 3.52 ± 0.41 µg/mg; CAT 245.8 ± 34.9, 175.1 ± 17.8, 222.6 ± 15.4 U/mg; SOD 103.2 ± 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; GSH 24.17 ± 3.37, 19.02 ± 3.78, 22.16 ± 3.31 mg/g; GPx 2.63 ± 0.98, 1.58 ± 0.30, 2.40 ± 0.48 µg/mg; CAT 95.33 ± 16.9, 65.50 ± 14.8, 92.30 ± 9.8 U/mg; SOD 12.1 ± 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

Certification: This paper should not enter any consumer-product occurrence pool. It is controlled animal toxicology and mechanistic evidence for lead acetate exposure, with measured Pb retention in kidney and testis and tissue-injury endpoints.

Courses: Useful for explaining why downstream toxicology papers belong in the corpus even when they do not measure a finished product: they document lead target-organ injury, oxidative stress, inflammation, and a co-treatment mechanism that did not reduce tissue Pb burden.

App: Supports lead toxicology context on the metal page. It does not support an ingredient contamination profile or a supplement-product occurrence row.

Microbiome: No microbiome endpoints.

Wiki pages this source may touch

• lead
• index

Verification notes

• Recovered under the 2026-06-10 inclusion-by-default rule, lane a4 exposure and health effect. Prior skip was skip:no-occurrence-data because the paper had no finished-product table.
• DOI, title, author list, journal, animal count, group size, Pb dose, vitamin D3 dose, kidney/testis Pb concentrations, serum Table 1, cytokine Table 2, oxidative-stress Table 3, and methods details were checked against the extracted PDF text on 2026-06-11.
• Units are preserved exactly as printed in the source: mg/L, IU/kg, µg/g, mg/dL, ng/mL, pg/mL, nmol/g, mg/g, µg/mg, and U/mg.
• Speciation: the source reports lead as Pb/lead acetate exposure and tissue Pb concentration; no lead speciation is reported.
• Products and ingredients are intentionally empty because this is an animal toxicology paper, not a supplement occurrence study.
• The vitamin D3 co-treatment improved multiple injury markers but did not significantly change tissue Pb concentrations; this distinction is preserved because it is load-bearing for remediation versus toxicity interpretation.

Page history

The five most recent substantive edits to this page. The full version history lives in git; when DOI minting comes online (see schema docs), each entry below will also link to a version-pinned DataCite DOI.