Effects of ATP and Taxifolin on Atezolizumab-Induced Renal Injury: A Biochemical, Histopathological, and Immunofluorescence Evaluation

ArticleAçık Erişim

Özet

Background: Immune checkpoint inhibitors (ICIs), particularly programmed death-ligand 1 (PD-L1) inhibitors such as atezolizumab, have significantly improved outcomes in cancer therapy. However, these agents may cause immune-related adverse effects, including nephrotoxicity associated with oxidative stress and cellular stress responses. This study aimed to investigate and comparatively evaluate the protective effects of adenosine triphosphate (ATP) and taxifolin against atezolizumab-induced renal tissue injury in rats. Methods: Animals were divided into four groups: healthy (HG), atezolizumab (ATZ), ATP + atezolizumab (ATAZ), and taxifolin + atezolizumab (TXAZ). ATP (4 mg/kg, i.p.) and taxifolin (50 mg/kg, oral) were administered for six days, while atezolizumab (10 mg/kg, i.p.) was given on days 1 and 4. On day 7, renal tissues were collected for biochemical, histopathological, and double immunofluorescence analyses. Results: Atezolizumab significantly increased malondialdehyde (MDA) levels and decreased total glutathione (tGSH), superoxide dismutase (SOD), and catalase (CAT) levels, indicating enhanced oxidative stress and impaired antioxidant defense. These changes were accompanied by tubular degeneration and increased expression of apoptotic markers. Both ATP and taxifolin significantly ameliorated these alterations; however, ATP demonstrated a more pronounced protective effect. Conclusions: In conclusion, ATP and taxifolin attenuated the biochemical, histopathological, and immunofluorescence alterations associated with atezolizumab administration. ATP exhibited a more pronounced protective effect than taxifolin under the conditions of this experimental model. Nevertheless, further experimental studies are required to elucidate the mechanisms underlying these effects. © 2026 by the authors.

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RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/10404Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.3390/life16071118Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorKilic, Adil Furkan
dc.contributor.authorSezgin, Esra Tuba
dc.contributor.authorHuseynova, Gulbaniz
dc.contributor.authorSarigul, Cengiz
dc.contributor.authorOzkaraca, Mustafa
dc.contributor.authorGungor, Ali
dc.contributor.authorMammadov, Renad
dc.contributor.authorSuleyman, Halis
dc.contributor.authorCimen, Orhan
dc.date.accessioned2026-10-18T20:25:37.545858965Z
dc.date.available2026-10-18T20:25:37.545858965Z
dc.date.issued2026
dc.description.abstractBackground: Immune checkpoint inhibitors (ICIs), particularly programmed death-ligand 1 (PD-L1) inhibitors such as atezolizumab, have significantly improved outcomes in cancer therapy. However, these agents may cause immune-related adverse effects, including nephrotoxicity associated with oxidative stress and cellular stress responses. This study aimed to investigate and comparatively evaluate the protective effects of adenosine triphosphate (ATP) and taxifolin against atezolizumab-induced renal tissue injury in rats. Methods: Animals were divided into four groups: healthy (HG), atezolizumab (ATZ), ATP + atezolizumab (ATAZ), and taxifolin + atezolizumab (TXAZ). ATP (4 mg/kg, i.p.) and taxifolin (50 mg/kg, oral) were administered for six days, while atezolizumab (10 mg/kg, i.p.) was given on days 1 and 4. On day 7, renal tissues were collected for biochemical, histopathological, and double immunofluorescence analyses. Results: Atezolizumab significantly increased malondialdehyde (MDA) levels and decreased total glutathione (tGSH), superoxide dismutase (SOD), and catalase (CAT) levels, indicating enhanced oxidative stress and impaired antioxidant defense. These changes were accompanied by tubular degeneration and increased expression of apoptotic markers. Both ATP and taxifolin significantly ameliorated these alterations; however, ATP demonstrated a more pronounced protective effect. Conclusions: In conclusion, ATP and taxifolin attenuated the biochemical, histopathological, and immunofluorescence alterations associated with atezolizumab administration. ATP exhibited a more pronounced protective effect than taxifolin under the conditions of this experimental model. Nevertheless, further experimental studies are required to elucidate the mechanisms underlying these effects. © 2026 by the authors.
dc.description.sponsorshipThis study received no external funding.
dc.identifier.doi10.3390/life16071118
dc.identifier.eissn2075-1729
dc.identifier.issn2075-1729
dc.identifier.issue7
dc.identifier.pmcidPMC13413056
dc.identifier.pmid42514188
dc.identifier.scopus2-s2.0-105045891477
dc.identifier.startpage1118
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/10404
dc.identifier.volume16
dc.identifier.wosWOS:001833597400001
dc.language.isoen
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI)
dc.relation.ispartofLife
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectantioxidant defense
dc.subjectapoptosis
dc.subjectatezolizumab
dc.subjectATP
dc.subjectnephrotoxicity
dc.subjectoxidative stress
dc.subjecttaxifolin
dc.subjectadenosine triphosphate
dc.subjectcatalase
dc.subjectglutathione
dc.subjectmalonaldehyde
dc.subjectsodium chloride
dc.subjectsuperoxide dismutase
dc.subjectthiopental
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcell stress
dc.subjectdrug efficacy
dc.subjectflow cytometry
dc.subjectimmunofluorescence
dc.subjectimmunohistochemistry
dc.subjectkidney injury
dc.subjectkidney tissue
dc.subjectmale
dc.subjectnonhuman
dc.subjectphysiological stress
dc.subjectrat
dc.titleEffects of ATP and Taxifolin on Atezolizumab-Induced Renal Injury: A Biochemical, Histopathological, and Immunofluorescence Evaluation
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus0
rdl.citation.wos0
rdl.departmentAnesthesia Program, Vocational School of Health Services, Erzincan Binali Yıldırım University, 24002 Erzincan, Turkey. | Department of Medical Biochemistry, Faculty of Medicine, Erzincan Binali Yıldırım University, 24100 Erzincan, Turkey. | Department of Pharmacology, Faculty of Medicine, Erzincan Binali Yıldırım University, 24100 Erzincan, Turkey. | Department of General Surgery, Faculty of Medicine, Erzincan Binali Yıldırım University, 24100 Erzincan, Turkey.
rdl.oa.statusgold
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)