Farahat et al. 2025 - Sinapic acid and cadmium hepatotoxicity in rats
Farahat and colleagues tested whether oral sinapic acid pretreatment mitigated acute cadmium-chloride liver injury in male Wistar rats. This is primary health/toxicology evidence, not food, ingredient, or product occurrence evidence. The routeable metal facts are the CdCl2 exposure dose, measured liver Cd accumulation, and downstream liver-function and oxidative-stress outcomes.
Key numbers
Exposure design and liver cadmium
The study used 40 mature male Wistar rats, 150-200 g body weight, randomized into four groups of ten animals. Group 1 received saline only. Group 2 received saline for 14 days followed by a single intraperitoneal CdCl2 dose of 3.5 mg/kg on day 14. Groups 3 and 4 received sinapic acid at 20 or 40 mg/kg/day by oral administration for 14 days, followed by the same 3.5 mg/kg intraperitoneal CdCl2 dose on day 14.
Figure 1 reports liver Cd concentration as mean +/- SD in ng/g tissue. The bars are not printed with numeric labels; graph-read approximate means are:
| Group | CdCl2 dose | Sinapic acid dose | Liver Cd, graph-read approximate (ng/g tissue) |
|---|---|---|---|
| Control | none | none | ~0.07 |
| CdCl2 + saline | 3.5 mg/kg IP once | none | ~1.17 |
| Sinapic acid + CdCl2 | 3.5 mg/kg IP once | 20 mg/kg/day PO | ~0.56 |
| Sinapic acid + CdCl2 | 3.5 mg/kg IP once | 40 mg/kg/day PO | ~0.18 |
The authors state that hepatic Cd was more than ten times higher in Cd-intoxicated animals than in controls, and that both sinapic acid doses significantly reduced hepatic Cd in a dose-dependent manner.
Liver function
Table 2 reports liver weight index, AST, and ALT as mean +/- SD:
| Endpoint | Control | CdCl2 + saline | Sinapic acid 20 mg/kg + CdCl2 | Sinapic acid 40 mg/kg + CdCl2 |
|---|---|---|---|---|
| Liver weight index | 3.3 +/- 0.0036 | 3.5 +/- 0.0053 | 3.7 +/- 0.0053 | 3.0 +/- 0.0044 |
| AST | 59.15 +/- 5.61 | 141.22 +/- 19.55 | 98.92 +/- 9.97 | 69.12 +/- 5.9 |
| ALT | 40.11 +/- 5.56 | 112.48 +/- 15.34 | 83.28 +/- 9.28 | 56.29 +/- 6.02 |
CdCl2 increased AST and ALT relative to control. Both sinapic acid doses reduced AST and ALT relative to the CdCl2-only group, with stronger improvement at 40 mg/kg.
Oxidative-stress markers
Table 3 reports oxidative-stress and Nrf2/HO-1 pathway markers as mean +/- SD:
| Endpoint | Control | CdCl2 + saline | Sinapic acid 20 mg/kg + CdCl2 | Sinapic acid 40 mg/kg + CdCl2 |
|---|---|---|---|---|
| MDA | 6.9 +/- 0.75 | 30.1 +/- 2.1 | 19.9 +/- 0.9 | 12.7 +/- 0.75 |
| GSH | 66.1 +/- 4.6 | 15.1 +/- 1.7 | 26.9 +/- 1.2 | 39.7 +/- 1.9 |
| SOD | 56.9 +/- 3.3 | 14.7 +/- 1.5 | 26.0 +/- 1.1 | 38.6 +/- 1.9 |
| CAT | 51.3 +/- 2.9 | 12.6 +/- 1.3 | 22.1 +/- 1.1 | 31.8 +/- 1.6 |
| Nrf2 | 1.0 +/- 0.1 | 0.39 +/- 0.05 | 0.62 +/- 0.07 | 0.85 +/- 0.1 |
| HO-1 | 29.55 +/- 1.26 | 6.55 +/- 0.63 | 12.62 +/- 0.46 | 22.13 +/- 0.88 |
The paper also reports that CdCl2 increased inflammatory, autophagy, MAPK, and apoptotic markers, while sinapic acid reduced TLR-4, NF-kB, TNF-alpha, COX-2, iNOS, IL-1beta, mTOR, JNK, ERK, p53, and BAX-associated injury patterns and improved Bcl-2 staining.
Methods (brief)
Rats were acclimated for one week and housed under controlled light, temperature, and humidity. Sinapic acid and CdCl2 were dissolved in isotonic saline. Blood was collected within 24 hours after CdCl2 administration for serum ALT and AST measurement. Liver tissue was dissected for histopathology, immunohistochemistry, biochemical marker assays, quantitative real-time PCR, and western blotting. Liver Cd and calcium were measured with sandwich ELISA kits following manufacturer instructions; oxidative-stress markers, inflammatory markers, and pathway proteins were measured by ELISA, qRT-PCR, immunohistochemistry, and western blot as applicable. Data were analyzed with one-way ANOVA and Bonferroni post hoc tests; histopathology scores used Kruskal-Wallis and Dunn tests.
Implications
Certification: This source does not support any HMTc product, ingredient, or market-occurrence distribution. It is a rodent acute-exposure toxicology model using intraperitoneal CdCl2, so it should remain in health context.
Courses: Useful mechanistic example for Cd hepatotoxicity: acute Cd increased liver Cd, serum AST/ALT, lipid peroxidation, inflammatory signaling, and apoptotic injury, while antioxidant pretreatment changed several downstream markers.
App: Route to cadmium health context only. Do not translate the sinapic-acid intervention into consumer supplement advice or product certification claims.
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Verification notes
The PDF has author attribution and DOI 10.3390/biomedicines13051065; no DOI conflict was observed. Figure 1 contains liver Cd bars and axis units but no printed numeric labels, so liver Cd concentrations are recorded as graph-read approximations and not treated as exact sample values. The study reports a cadmium chloride toxicology challenge, not food-chain Cd occurrence. The paper mentions sinapic acid as a plant-derived compound found in foods, but it does not measure metals in foods, ingredients, supplements, or consumer products.
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.
| Commit | Date | Description |
|---|---|---|
| c1aef38 | 2026-06-02 | audit-queue: hamid2021-bacterial-plant-biostimulants-review → audited-promote |