Related Experiment Video
Updated: Aug 7, 2026

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
Published on: January 7, 2013
Ozone/oxygen mixture modifies the subcellular redistribution of Bax protein in renal tissue from rats treated with
Aluet Borrego1, Zullyt Barbara Zamora, Ricardo González
1National Laboratory for the Control of Drugs, Center for the Control and Development of Drugs, Havana, Cuba. aluetborrego@yahoo.com
Background:
Cellular events in cisplatin-mediated nephrotoxicity include apoptosis induction, decreased protein synthesis, changes in the subcellular redistribution of Bax mitochondrial dysfunction, DNA injury, increased lipid peroxidation, depletion of glutathione and decrease in enzymatic activity of renal antioxidant enzymes. In previous papers we have shown that intra-rectal (i.r.) ozone/oxygen mixture protected and induced a significant recovery in cisplatin-induced renal damage and was related to a significant increase in the antioxidant system in renal tissue.
Methods:
This study was undertaken to examine the effect of the ir applications of ozone/oxygen mixture in the renal expression pattern of Bax proteins in rats treated with cisplatin. A group of male Sprague-Dawley rats was pretreated with 15 i.r. applications of ozone/oxygen (1.1 mg/kg) before intraperitoneal injection of cisplatin (6 mg/kg). Another group was treated with five i.r. applications of ozone/oxygen mixture after cisplatin administration. Serum creatinine was measured thereafter. Subcellular distribution of Bax in renal tissue was analyzed by immunohistochemistry.
Results:
Ozone pretreatment prevented the increase in serum creatinine levels and completely inhibited the acute tubular necrosis induced by cisplatin in renal tissue, diminishing the expression of Bax. Ozone treatment after cisplatin application reduced the increase in serum creatinine levels and the renal necrosis, inducing a lesser decrease of the Bax expression in cisplatin-treated kidneys.
Conclusions:
Expression of Bax in renal tissue seems to play an important role in the protection and recovery in cisplatin-nephrotoxicity achieved by ozone/oxygen mixture.
Insights
Ozone/oxygen therapy protects against cisplatin-induced kidney damage by modulating Bax protein expression. Pretreatment with ozone/oxygen prevented damage, while post-treatment aided recovery, highlighting its therapeutic potential.
Area of Science:
- Nephrology
- Biochemistry
- Toxicology
Background:
- Cisplatin chemotherapy causes kidney damage via apoptosis, DNA injury, and oxidative stress.
- Ozone/oxygen mixture has previously shown protective effects against cisplatin-induced renal damage.
- This protection is linked to an enhanced renal antioxidant system.
Purpose of the Study:
- To investigate the impact of intra-rectal ozone/oxygen mixture on renal Bax protein expression in cisplatin-treated rats.
- To evaluate the protective and recovery effects of ozone/oxygen therapy on cisplatin nephrotoxicity.
Main Methods:
- Male Sprague-Dawley rats received either ozone/oxygen pretreatment or post-treatment relative to cisplatin administration.
- Serum creatinine levels were measured to assess kidney function.
- Immunohistochemistry was used to analyze Bax protein expression and subcellular distribution in renal tissue.
Main Results:
- Ozone/oxygen pretreatment completely prevented cisplatin-induced acute tubular necrosis and increased serum creatinine, while diminishing Bax expression.
- Post-treatment with ozone/oxygen reduced cisplatin-induced renal necrosis and serum creatinine increase, with a less pronounced reduction in Bax expression.
- These findings suggest Bax protein plays a key role in ozone/oxygen's protective effects.
Conclusions:
- Ozone/oxygen mixture demonstrates significant protective and recovery effects against cisplatin nephrotoxicity.
- Modulation of Bax protein expression in renal tissue is central to the therapeutic benefits of ozone/oxygen therapy.
- Ozone/oxygen therapy represents a promising strategy for mitigating cisplatin-induced kidney injury.

