Evidence map›Paper›PMID 40742482›Full record

ArticleAmino acids2025

Protective effects of S-adenosyl methionine on oxidative stress and tissue damage in STZ-induced diabetic rats.

AmirHossein RahimBakhsh, Asma Kheirollahi, Akram Vatannejad, Sara Shokrpoor, Rahman Mohammadi

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Article in Amino acids, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

AmirHossein RahimBakhshDepartment of Comparative Biosciences, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.
Asma KheirollahiDepartment of Comparative Biosciences, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran. kheirolahi_asma@ut.ac.ir.
Akram VatannejadDepartment of Comparative Biosciences, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.
Sara ShokrpoorDepartment of Pathology and Clinical Pathology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.
Rahman MohammadiDepartment of Comparative Biosciences, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOxidative stress is a key contributor to the progression of diabetes mellitus and its associated complications. Recently, S-adenosyl methionine (SAM) has shown promise in mitigating oxidative stress and improving glucose metabolism. This study aimed to investigate the effects of SAM supplementation on biochemical parameters, oxidative stress markers, and histopathological alterations in the kidneys and liver of streptozotocin (STZ)-induced diabetic rats.

methodsEighteen male Wistar rats were randomly divided into three groups (n = 6 per group): non-diabetic control, diabetic control, and diabetic rats treated with SAM (10 mg/kg/day, intraperitoneally) for 4 weeks. Fasting blood glucose, renal and hepatic biochemical markers (urea, creatinine, ALT, AST), and oxidative stress markers (malondialdehyde, protein carbonyls, total antioxidant capacity) were measured. Histopathological changes in kidney and liver tissues were also assessed.

resultsDiabetic rats treated with SAM exhibited minor, non-significant changes in fasting blood glucose, urea, creatinine, ALT, and AST levels. In contrast, treatment with SAM in diabetic rats significantly reduced malondialdehyde and protein carbonyl levels in both kidney and liver tissues compared to the diabetic control group (P < 0.05). Furthermore, histopathological analysis revealed improved tissue architecture and reduced pathological changes in the diabetic group treated with SAM.

conclusionOur findings demonstrated that SAM supplementation exerts significant antioxidant and histopathological protective effects against diabetes-induced damage in kidney and liver tissues.

Indexed as

AntioxidantsDiabetes Mellitus, ExperimentalOxidative StressS-AdenosylmethionineAnimalsBlood GlucoseKidneyLiverMaleRatsRats, WistarStreptozocinAntioxidantsBlood GlucoseS-AdenosylmethionineStreptozocinDiabetesGlucose homeostasisOxidative stressS-adenosyl methionine

Identifiers

PMID40742482
PMCPMC12313745

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.