Effects of adenosine triphosphate and reduced glutathione on biochemical, histopathological and immunofluorescence alterations associated with atezolizumab-induced cardiac tissue injury

Q: What are the key findings of this study?

Adenosine triphosphate and reduced glutathione significantly attenuated biochemical, histopathological, and immunofluorescence alterations associated with atezolizumab-induced cardiac injury in rats.

Q: What is the clinical evidence from this study?

Population: Atezolizumab-induced cardiac tissue injury (n=24). Intervention: Adenosine triphosphate (ATP) and reduced glutathione (GSH) vs. Atezolizumab alone and healthy controls. Primary outcome: Biochemical markers of oxidative stress and inflammation (MDA, tGSH, SOD, catalase, IL-1β, IL-6) in heart tissue (p=<0.001).

Q: What does this research mean for the field?

Adenosine triphosphate (ATP) and reduced glutathione (GSH) significantly attenuate oxidative stress, inflammation, and cardiac tissue injury induced by atezolizumab in a rat model. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To investigate whether adenosine triphosphate (ATP) and reduced glutathione (GSH) provide protective effects against atezolizumab-induced cardiac tissue injury in a rat model.

Yesim Kaya Yasar; Esra Tuba Sezgin; Bahadır Süleyman; Renad Mammadov; Mustafa Özkaraca; Ali Güngör; Taha Abdulkadir Çoban; Halis Süleyman

doi:10.3389/fphar.2026.1914819

September 4, 2026Frontiers in PharmacologyOpen Access

Effects of adenosine triphosphate and reduced glutathione on biochemical, histopathological and immunofluorescence alterations associated with atezolizumab-induced cardiac tissue injury

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Key result

ATP and GSH attenuate atezolizumab-induced cardiac injury in rats.

P<0.001
n=24

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Why the study?

The study investigated the potential protective effects of adenosine triphosphate and glutathione against atezolizumab-induced cardiac injury in rat heart tissue.

Do adenosine triphosphate (ATP) and reduced glutathione (GSH) prevent atezolizumab-induced cardiac tissue injury in a rat model?

Key Points

To investigate whether adenosine triphosphate (ATP) and reduced glutathione (GSH) provide protective effects against atezolizumab-induced cardiac tissue injury in a rat model.
A total of 24 male albino Wistar rats were divided into four groups (n = 6 per group): healthy control, ATP + atezolizumab (ATAZ), GSH + atezolizumab (GHAZ), and atezolizumab alone (ATZ).
ATP was administered intraperitoneally at 4 mg/kg daily, oral GSH was administered at 200 mg/kg daily for 7 days, and atezolizumab was given intraperitoneally at 10 mg/kg twice weekly.
Myocardial tissue was evaluated for malondialdehyde, total glutathione, superoxide dismutase, catalase, interleukin-1β, and interleukin-6 levels alongside histopathological and immunofluorescence analyses.
Atezolizumab exposure increased cardiac markers of oxidative stress (malondialdehyde) and inflammatory cytokines (interleukin-1β, interleukin-6) while reducing total glutathione, superoxide dismutase, and catalase activities.
Coadministration of ATP (4 mg/kg) or GSH (200 mg/kg) significantly attenuated oxidative stress and inflammatory increases while restoring myocardial antioxidant enzyme activities.
Histopathological and immunofluorescence evaluations demonstrated that both ATP and GSH ameliorated atezolizumab-induced structural heart tissue damage.

Structured PICO

Do adenosine triphosphate (ATP) and reduced glutathione (GSH) prevent atezolizumab-induced cardiac tissue injury in a rat model?

P

Population

24 male albino Wistar rats weighing 280-290 g subjected to an experimental model of atezolizumab-induced cardiac injury for 7 days.

I

Intervention

Adenosine triphosphate (ATP) 4 mg/kg intraperitoneally once daily for 7 days, or reduced glutathione (GSH) 200 mg/kg orally once daily for 7 days, administered alongside atezolizumab 10 mg/kg intraperitoneally twice weekly (on days 1 and 4).

C

Comparator

Atezolizumab alone (10 mg/kg intraperitoneally twice weekly) plus vehicle (distilled water), and a healthy control group receiving vehicle only.

O

Outcome

Levels of malondialdehyde (MDA), total glutathione (tGSH), superoxide dismutase (SOD), catalase, interleukin-1β (IL-1β), and interleukin-6 (IL-6) in heart tissues at 7 days.surrogate

Main Result

p-value: p=<0.001

In a rat model, ATP and GSH significantly attenuated oxidative stress, inflammation, and histopathological damage associated with atezolizumab-induced cardiac injury.

Limitations

Use of an experimental animal model restricts direct translation to clinical settings.
Only male rats were included, preventing evaluation of sex-related differences.
Short duration of the study limited evaluation of long-term cardiotoxic effects.
Absence of ATP-alone and GSH-alone groups prevented discrimination of intrinsic biological effects.
Mitochondrial function and ATP levels in cardiac tissue were not measured.
Small sample size without a priori power analysis.
A formal a priori power analysis was not performed prior to the study
Direct evidence demonstrating functional binding of atezolizumab to rat PD-L1 remains limited
Mitochondrial function was not evaluated

Ask about this paper

Answers are grounded in this paper and cite their sources.

Implication

Does not support clinical use of ATP or glutathione with atezolizumab; leaves open further preclinical validation.

Abstract

Background In this study, the potential protective effects of adenosine triphosphate (ATP) and glutathione (GSH) against atezolizumab-induced cardiac injury in rat heart tissue were investigated. Methods A total of 24 male albino Wistar rats were used in the experiment. The animals were divided into four groups: healthy group adenosine triphosphate + atezolizumab (ATAZ), GSH + atezolizumab (GHAZ), and atezolizumab alone (ATZ). ATP was administered intraperitoneally at a dose of 4 mg/kg, while GSH was administered orally at a dose of 200 mg/kg for 7 days. Atezolizumab was administered intraperitoneally to the experimental groups at a dose of 10 mg/kg twice weekly. At the end of the experiment, malondialdehyde total glutathione (tGSH), superoxide dismutase catalase, interleukin-1β (IL-1β), and interleukin-6 (IL-6) levels in heart tissues were measured using biochemical methods. In addition, histopathological and immunofluorescence examinations were performed. Results The results showed that oxidative stress and inflammation markers increased, whereas antioxidant parameters decreased in the atezolizumab-treated group. ATP and GSH administration significantly attenuated these changes and exerted protective effects on cardiac tissue. Conclusion Overall, ATP and GSH ameliorated the biochemical, histopathological, and immunofluorescence changes associated with atezolizumab-induced cardiac injury in this experimental model.

Discussion

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Cite This Study

Yasar et al. (2026) studied Atezolizumab-induced cardiac tissue injury (n=24). Adenosine triphosphate (ATP) and reduced glutathione (GSH) vs. Atezolizumab alone and healthy controls was evaluated on Biochemical markers of oxidative stress and inflammation (MDA, tGSH, SOD, catalase, IL-1β, IL-6) in heart tissue (p=<0.001). Adenosine triphosphate and reduced glutathione significantly attenuated biochemical, histopathological, and immunofluorescence alterations associated with atezolizumab-induced cardiac injury in rats.

synapsesocial.com/papers/6a9fafb81311c3d51b618455 https://doi.org/10.3389/fphar.2026.1914819

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Effects of adenosine triphosphate and reduced glutathione on biochemical, histopathological and immunofluorescence alterations associated with atezolizumab-induced cardiac tissue injury

Figures

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Effects of adenosine triphosphate and reduced glutathione on biochemical, histopathological and immunofluorescence alterations associated with atezolizumab-induced cardiac tissue injury

Figures

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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