The Protective Role of Ozone Therapy in Kidney Disease: A Review

Delgadillo-Valero, Luis Fernando; Hernández-Cruz, Estefani Yaquelin; Pedraza-Chaverri, José

doi:10.3390/life13030752

Cited by 7 publications

(5 citation statements)

References 89 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lower dosages (50 or 100 mg/kg) or shorter periods (5 or 7 days) are almost without histochemical and biochemical consequences. It has been reported that the nephrotoxicity induced by GN involves different pathways, including oxidative stress (OS), inflammation, nitric oxide (NO) generation, lipid peroxidation, and decreased efficiency of kidney antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione peroxidase, and reduced glutathione (GSH) levels [21]. This is in accordance with the results obtained in our study, which revealed that the GN-treated group had increased (OS) by depleting the activity of antioxidant enzymes and showing a drastic increase in ROS/RNS levels, leading to protein damage and increased levels of inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

Vitamin E and Silymarin Reduce Oxidative Tissue Damage during Gentamycin-Induced Nephrotoxicity

Georgiev,

Nikolova,

Dyakova

et al. 2023

Pharmaceuticals

View full text Add to dashboard Cite

Aminoglycoside antibiotics and gentamicin (GN), in particular, are still widely used in clinical practice. It is a well-known fact that GN causes nephrotoxicity, and redox disturbances are discussed as a factor in its side effects. Recently, a new type of cell oxidative death, named ferroptosis, was discovered; it is associated with iron accumulation in the cell, glutathione (GSH) depletion and inactivation of glutathione peroxidase-4 (GPX4), reactive oxygen species (ROS) increment with concomitant lipid peroxidation. In this regard, a possible connection between GN-induced renal damage, ferroptosis and the overall antioxidant status of the organism could be investigated. Moreover, due to its beneficial effects, GN is still one of the main choices as a therapeutic agent for several diseases, and the possible reduction of its side effects with the application of certain antioxidants will be of important clinical significance. The study was conducted with adult male white mice divided into several groups (n = 6). GN nephrotoxicity was induced by the administration of GN 100–200 mg/kg i.p. for 10 days. The control group received only saline. The other groups received either Vitamin E (400 mg/kg p.o.) or Silymarin (200 mg/kg p.o.) applied alone or together with GN for the same period. After the end of the study, the animals were sacrificed, and blood and tissue samples were taken for the assessment of biochemical parameters and antioxidant status, as well as routine and specific for GPX4 histochemistry examination. The experimental results indicate that GN-induced nephrotoxicity negatively modulates GPX4 activity and is associated with increased production of ROS and lipid peroxidation. The groups treated with antioxidants demonstrated preserved antioxidant status and better GPX4 activity. In conclusion, the inhibition of ROS production and especially the suppression of ferroptosis, could be of clinical potential and can be applied as a means of reducing the toxic effects of GN application.

show abstract

Section: Discussionmentioning

confidence: 99%

Vitamin E and Silymarin Reduce Oxidative Tissue Damage during Gentamycin-Induced Nephrotoxicity

Georgiev,

Nikolova,

Dyakova

et al. 2023

Pharmaceuticals

View full text Add to dashboard Cite

show abstract

“…Although some previous studies have found a negative correlation between O 3 and the rate of decline in kidney function, this result needs to be interpreted with caution. [ 35 ]…”

Section: Discussionmentioning

confidence: 99%

“…Although some previous studies have found a negative correlation between O 3 and the rate of decline in kidney function, this result needs to be interpreted with caution. [35] F I G U R E 2 Forest plot of the association between O 3 exposure and CKD risk. The size of the gray boxes for each point estimate represents the size of the included study.…”

Section: Principal Findingsmentioning

confidence: 99%

Association of air pollution and risk of chronic kidney disease: A systematic review and meta‐analysis

Xu,

Jia,

Lin

et al. 2023

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Although epidemiological studies have evaluated the association between ambient air pollution and chronic kidney disease (CKD), the results remain mixed. To clarify the nature of the association, we conducted a comprehensive systematic review and meta‐analysis to assess the global relationship between air pollution and CKD. The Web of Science, PubMed, Embase and Cochrane Library databases systematically were searched for studies published up to July 2023 and included 32 studies that met specific criteria. The random effects model was used to derive overall risk estimates for each pollutant. The meta‐analysis estimated odds ratio (ORs) of risk for CKD were 1.42 (95% confidence interval [CI]: 1.31–1.54) for each 10 μg/m3 increase in PM2.5; 1.20 (95% CI: 1.14–1.26) for each 10 μg/m3 increase in PM10; 1.07 (95% CI: 1.05–1.09) for each 10 μg/m3 increase in NO2; 1.03 (95% CI: 1.02–1.03) for each 10 μg/m3 increase in NOX; 1.07 (95% CI: 1.01–1.12) for each 1 ppb increase in SO2; 1.03 (95% CI: 1.00–1.05) for each 0.1 ppm increase in CO. Subgroup analysis showed that this effect varied by gender ratio, age, study design, exposure assessment method, and income level. Furthermore, PM2.5, PM10, and NO2 had negative effects on CKD even within the World Health Organization‐recommended acceptable concentrations. Our results further confirmed the adverse effect of air pollution on the risk of CKD. These findings can contribute to enhance the awareness of the importance of reducing air pollution among public health officials and policymakers.

show abstract

“…However, study on the effects of O 3 on the renal outcome and mortality in chronic kidney disease (CKD) is lacking. While it has been observed that there is a correlation between long-term exposure to O 3 and the prevalence of CKD, as well as an inverse correlation with eGFR [ 13 , 14 ], some experimental studies have reported that O 3 may play a role in the treatment of kidney disease [ 15 ]. Therefore, further research is needed to determine whether long-term exposure to O 3 affects the long-term prognosis of CKD.…”

Section: Introductionmentioning

confidence: 99%

Long-term ozone exposure and mortality in patients with chronic kidney disease: a large cohort study

Kim,

Huh,

et al. 2024

BMC Nephrol

View full text Add to dashboard Cite

Background Epidemiologic studies on the effects of long-term exposure to ozone (O3) have shown inconclusive results. It is unclear whether to O3 has an effect on chronic kidney disease (CKD). We investigated the effects of O3 on mortality and renal outcome in CKD. Methods We included 61,073 participants and applied Cox proportional hazards models to examine the effects of ozone on the risk of end-stage renal disease (ESRD) and mortality in a two-pollutants model adjusted for socioeconomic status. We calculated the concentration of ozone exposure one year before enrollment and used inverse distance weighting (IDW) for interpolation, where the exposure was evenly distributed. Results In the single pollutant model, O3 was significantly associated with an increased risk of ESRD and all-cause mortality. Based on the O3 concentration from IDW interpolation, this moving O3 average was significantly associated with an increased risk of ESRD and all-cause mortality. In a two-pollutants model, even after we adjusted for other measured pollutants, nitrogen dioxide did not attenuate the result for O3. The hazard ratio (HR) value for the district-level assessment is 1.025 with a 95% confidence interval (CI) of 1.014–1.035, while for the point-level assessment, the HR value is 1.04 with a 95% CI of 1.035–1.045. The impact of ozone on ESRD, hazard ratio (HR) values are, 1.049(95%CI: 1.044–1.054) at the district unit and 1.04 (95%CI: 1.031–1.05) at the individual address of the exposure assessment. The ozone hazard ratio for all-cause mortality was 1.012 (95% confidence interval: 1.008–1.017) for administrative districts and 1.04 (95% confidence interval: 1.031–1.05) for individual addresses. Conclusions This study suggests that long-term ambient O3 increases the risk of ESRD and mortality in CKD. The strategy to decrease O3 emissions will substantially benefit health and the environment.

show abstract

The Protective Role of Ozone Therapy in Kidney Disease: A Review

Cited by 7 publications

References 89 publications

Vitamin E and Silymarin Reduce Oxidative Tissue Damage during Gentamycin-Induced Nephrotoxicity

Vitamin E and Silymarin Reduce Oxidative Tissue Damage during Gentamycin-Induced Nephrotoxicity

Association of air pollution and risk of chronic kidney disease: A systematic review and meta‐analysis

Long-term ozone exposure and mortality in patients with chronic kidney disease: a large cohort study

Contact Info

Product

Resources

About