What is the clinical evidence from this study?

Study design: Other. Population: Cisplatin-induced hepatotoxicity (n=16). Intervention: Cisplatin vs. Saline solution. Primary outcome: Hepatotoxicity (ALT and AST levels), mitochondrial structure/function, and apoptosis.

What does this research mean for the field?

Cisplatin administration induces hepatotoxicity characterized by mitochondrial oxidative stress, membrane rigidification, energetic metabolism impairment, and apoptotic cell death in rat liver. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To evaluate the in vivo impact of cisplatin on hepatic mitochondrial structure, energetic function, and apoptosis in rat liver tissue.

June 29, 2007Journal of Applied Toxicology

Cisplatin induces mitochondrial oxidative stress with resultant energetic metabolism impairment, membrane rigidification and apoptosis in rat liver

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Key result

Cisplatin induces hepatotoxicity in rats, characterized by mitochondrial rigidification, oxidative stress, and apoptosis.

n=16

Why the study?

Does cisplatin induce hepatotoxicity via mitochondrial oxidative stress and apoptosis in adult male Wistar rats?

Population

Adult male Wistar rats (200-220 g), n=16

Comparison

Cisplatin (10 mg kg(-1) body weight, i.p.) vs Control group (saline solution, 1 ml 100 g body…

Design

Preclinical, divided into two groups

Follow-up

72 h

Authors

NMNádia Maria MartinsUniversidade de São Paulo NSNeife Aparecida Guinaim dos SantosUniversidade de Ribeirão Preto CCCarlos CurtiUniversidade de Ribeirão Preto

Discussion

Member takes

Implication

Identifies mitochondrial targets for cytoprotection in cisplatin hepatotoxicity; hypothesis-generating in rats, no clinical implications yet.

Key Points

To evaluate the in vivo impact of cisplatin on hepatic mitochondrial structure, energetic function, and apoptosis in rat liver tissue.
Adult male Wistar rats (200–220 g, n=8 per group) were administered a single intraperitoneal dose of either saline (control) or cisplatin (10 mg/kg).
Animals were sacrificed 72 hours after injection to assess circulating liver enzymes, mitochondrial oxidative parameters, and apoptotic markers.
Cisplatin exposure induced marked hepatotoxicity, demonstrated by significant elevations in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST).
Hepatic mitochondria displayed membrane rigidification, extensive lipid peroxidation, cardiolipin oxidation, protein sulfhydryl loss, and depletion of ATP, GSH, and NADPH.
Cisplatin promoted hepatocellular death through apoptosis driven by the mitochondrial signaling pathway.

Structured PICO

Does cisplatin induce hepatotoxicity via mitochondrial oxidative stress and apoptosis in adult male Wistar rats?

Population

16 adult male Wistar rats treated with cisplatin or saline to evaluate hepatotoxicity and mitochondrial oxidative stress at 72 hours.

Intervention

Cisplatin (10 mg kg(-1) body weight, i.p.)

Comparator

Control group (saline solution, 1 ml 100 g(-1) body weight, i.p.)

Outcome

Cisplatin-induced effects on hepatic mitochondrial structure and function as well as the occurrence of hepatocellular death by apoptosissurrogate

Cisplatin induces hepatotoxicity in rats through mitochondrial oxidative stress, energetic metabolism impairment, and apoptosis, highlighting potential targets for cytoprotective therapies.

Cite This Study

Martins et al. (2007) studied Cisplatin-induced hepatotoxicity (n=16). Cisplatin vs. Saline solution was evaluated on Hepatotoxicity (ALT and AST levels), mitochondrial structure/function, and apoptosis. Cisplatin administration in rats induced hepatotoxicity, characterized by increased ALT and AST, mitochondrial membrane rigidification, oxidative stress, and apoptosis.

synapsesocial.com/papers/6aa8fa71b7c808b8b5d91f16 https://doi.org/10.1002/jat.1284

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Implication

Identifies mitochondrial targets for cytoprotection in cisplatin hepatotoxicity; hypothesis-generating in rats, no clinical implications yet.

Cisplatin induces mitochondrial oxidative stress with resultant energetic metabolism impairment, membrane rigidification and apoptosis in rat liver

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Cisplatin induces mitochondrial oxidative stress with resultant energetic metabolism impairment, membrane rigidification and apoptosis in rat liver

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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