Protective Role of Astaxanthin Against Bisphenol A Induced Biochemical and Histopathological Alterations in Rat Kidneys

dc.contributor.author Gultekin, Burcu
dc.contributor.author Karabekir, Seda Cetinkaya
dc.contributor.author Ayan, Ilknur Cinar
dc.contributor.author Sava, Hasan Basri
dc.contributor.author Kalkan, Serpil
dc.date.accessioned 2025-11-15T15:11:41Z
dc.date.available 2025-11-15T15:11:41Z
dc.date.issued 2025
dc.description.abstract Objective(s): This study investigates the ability of astaxanthin (ASTX), a powerful anti-oxidant, to protect kidney tissue from oxidative and cellular damage resulting from bisphenol A (BPA) toxicity, a widespread global toxin associated with chronic kidney disease. Materials and Methods: We used 32 male Wistar Albino rats, 16 weeks old, and weighing 250-300 g. The rats were randomly divided into four groups: Control, Sham, BPA, and BPA+ASTX. Following the experiment, serum samples were assessed for Paraoxonase 1 (PON1), Arylesterase (ARE), urea, and creatinine levels. Changes in kidney tissue induced by BPA were examined using histopathological methods. Also, the levels of apoptosis and collagen content were evaluated. Results: ASTX treatment reversed the BPA-induced inhibition of PON1 and ARE levels, restoring them to control levels, and reduced the BPA-induced increase in urea levels. Creatinine levels showed no significant differences across the groups. BPA exposure in kidney tissue caused vacuolization, congestion, tubular dilatation, desquamation, infiltration, and increased collagen around glomeruli and blood vessels. However, ASTX treatment significantly improved these pathological findings. While BPA induced apoptosis as indicated by Bax and Bcl-2 analysis, ASTX treatment partially inhibited this process. Conclusion: These findings indicate that ASTX may protect against BPA-induced renal injury. However, the study's limitations include the use of a single dose and a focus solely on kidney tissue. Additionally, the lack of dose-response data and evaluations of other organs or long-term effects are significant drawbacks. Future research should explore multiple doses and longer observation periods for a better understanding of ASTX's protective efficacy. en_US
dc.description.sponsorship Necmettin Erbakan University Research Projects Office [211218026] en_US
dc.description.sponsorship This work was supported by Necmettin Erbakan University Research Projects Office (Grant number 211218026) . en_US
dc.identifier.doi 10.22038/ijbms.2025.88356.19081
dc.identifier.issn 2008-3866
dc.identifier.issn 2008-3874
dc.identifier.scopus 2-s2.0-105019800981
dc.identifier.uri https://doi.org/10.22038/ijbms.2025.88356.19081
dc.identifier.uri https://hdl.handle.net/20.500.12514/9915
dc.language.iso en en_US
dc.publisher Mashhad Univ Med Sciences en_US
dc.relation.ispartof Iranian Journal of Basic Medical Sciences en_US
dc.rights info:eu-repo/semantics/closedAccess en_US
dc.subject Apoptosis en_US
dc.subject Astaxanthin en_US
dc.subject Bisphenol A en_US
dc.subject Kidney Diseases en_US
dc.subject Oxidative Stress en_US
dc.title Protective Role of Astaxanthin Against Bisphenol A Induced Biochemical and Histopathological Alterations in Rat Kidneys en_US
dc.type Article en_US
dspace.entity.type Publication
gdc.author.scopusid 58097475200
gdc.author.scopusid 57215221212
gdc.author.scopusid 57218209715
gdc.author.scopusid 56562721800
gdc.author.scopusid 6603466606
gdc.description.department Artuklu University en_US
gdc.description.departmenttemp [Gultekin, Burcu; Kalkan, Serpil] Necmettin Erbakan Univ, Fac Med, Dept Histol & Embryol, Konya, Turkiye; [Karabekir, Seda Cetinkaya] Bakircay Univ, Fac Med, Dept Histol & Embryol, Izmir, Turkiye; [Ayan, Ilknur Cinar] Necmettin Erbakan Univ, Fac Med, Dept Med Biol, Konya, Turkiye; [Sava, Hasan Basri] Mardin Artuklu Univ, Fac Med, Dept Med Biochem, Mardin, Turkiye en_US
gdc.description.endpage 1655 en_US
gdc.description.issue 12 en_US
gdc.description.publicationcategory Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı en_US
gdc.description.scopusquality Q3
gdc.description.startpage 1647 en_US
gdc.description.volume 28 en_US
gdc.description.woscitationindex Science Citation Index Expanded
gdc.description.wosquality Q2
gdc.identifier.wos WOS:001605565100005
gdc.opencitations.count 0
gdc.plumx.scopuscites 0
gdc.scopus.citedcount 0
gdc.wos.citedcount 0

Files