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Evaluation of Liver Function Through SGOT and SGPT Quantification in Rats Administered Polyethylene Terephthalate Microplastics

Journal of Medical Laboratory in Infectious and Degenerative Diseases 2025 Score: 48 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Diana Nadhifah, Hartalina Mufidah, Ahdiah Imroatul Muflihah

Summary

Researchers administered PET microplastics orally to white rats at doses of 0.4–1.0 mg/day and measured SGOT and SGPT liver enzyme levels, finding dose-dependent increases in both transaminases indicating hepatotoxicity even at low exposure levels.

Polymers
Body Systems
Models

Background: Microplastics, as emerging environmental pollutants, can accumulate in target organs such as the liver and induce hepatotoxicity through oxidative stress mechanisms. Purpose: To determine the effect of PET microplastic exposure at various doses on liver transaminase enzyme levels (SGOT and SGPT) in white rats. Methods: This experimental study used 25 male white rats (Rattus norvegicus), aged 8–10 weeks, divided into five groups (n=5 per group): control (distilled water), P1 (0.4 mg/day), P2 (0.6 mg/day), P3 (0.8 mg/day), and P4 (1.0 mg/day) of orally administered PET microplastics for 28 days. SGOT and SGPT levels were measured using spectrophotometry. Statistical analysis was performed using ANOVA followed by Tukey-HSD or Bonferroni post hoc tests (α=0.05). Results: The SGPT level in the control group (61.48 ± 7.50 U/L) significantly increased to 114.40 ± 7.71 U/L (P1), 132.22 ± 18.41 U/L (P2), 191.78 ± 16.42 U/L (P3), and 227.26 ± 12.23 U/L (P4). The SGOT level in the control group (78.64 ± 9.48 U/L) significantly increased to 188.46 ± 2.55 U/L (P1), 195.10 ± 5.75 U/L (P2), 238.90 ± 41.34 U/L (P3), and 310.74 ± 26.66 U/L (P4). Statistical analysis revealed significant differences among groups (p < 0.05). The higher the PET microplastic dose, the higher the SGOT and SGPT levels observed. Conclusions: ET microplastic exposure induces hepatotoxicity, as evidenced by dose-dependent increases in SGOT and SGPT levels.

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