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<p>Trimethyltin (TMT) is widely used to model hippocampal degeneration in rodents, but its effects on the kidney are poorly understood. This study investigated renal function, histology, inflammation, and Klotho expression in TMT-exposed rats. Ten male Sprague–Dawley rats (8–10 weeks) were divided into control and TMT groups (<i>n</i> = 5 each). TMT-treated rats received a single intraperitoneal dose (8&#xa0;mg/kg). On day 28, serum urea and creatinine were measured. Kidney morphology was examined by Hematoxylin–Eosin and Periodic Acid Schiff staining. TNF-α and Klotho localization were assessed by immunohistochemistry, and Klotho and Nrf2 mRNA levels were quantified by qPCR. Body weight and renal function were similar between groups, indicating preserved kidney function. Histology revealed mild inflammatory cell infiltration in TMT-exposed kidneys and PAS staining showed mesangial expansion. TNF-α expression increased in distal tubules, while Klotho protein was elevated in cortical distal and medullary tubules, with higher semiquantitative scores than controls. Klotho and Nrf2 mRNA levels remained unchanged, suggesting post-transcriptional regulation. At 28 days post-TMT exposure, kidneys showed mild inflammation without functional impairment. Increased Klotho protein likely reflects a compensatory adaptive response to stress, indicating renal protective mechanisms following systemic TMT toxicity.</p>

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Upregulated Klotho expression reflects a potential compensatory renal response in Trimethyltin-exposed rats

  • 期刊论文

  • 发表日期：

    2026年3月26日

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  • Devi Purnamasari Sasongko,
  • Dian Eurike Septyaningtrias,
  • Rina Susilowati

摘要

Trimethyltin (TMT) is widely used to model hippocampal degeneration in rodents, but its effects on the kidney are poorly understood. This study investigated renal function, histology, inflammation, and Klotho expression in TMT-exposed rats. Ten male Sprague–Dawley rats (8–10 weeks) were divided into control and TMT groups (n = 5 each). TMT-treated rats received a single intraperitoneal dose (8 mg/kg). On day 28, serum urea and creatinine were measured. Kidney morphology was examined by Hematoxylin–Eosin and Periodic Acid Schiff staining. TNF-α and Klotho localization were assessed by immunohistochemistry, and Klotho and Nrf2 mRNA levels were quantified by qPCR. Body weight and renal function were similar between groups, indicating preserved kidney function. Histology revealed mild inflammatory cell infiltration in TMT-exposed kidneys and PAS staining showed mesangial expansion. TNF-α expression increased in distal tubules, while Klotho protein was elevated in cortical distal and medullary tubules, with higher semiquantitative scores than controls. Klotho and Nrf2 mRNA levels remained unchanged, suggesting post-transcriptional regulation. At 28 days post-TMT exposure, kidneys showed mild inflammation without functional impairment. Increased Klotho protein likely reflects a compensatory adaptive response to stress, indicating renal protective mechanisms following systemic TMT toxicity.