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Ceftriaxone-vancomycin drug toxicity reduction by VRP 1020 in Mus musculus mice
Arvind Soni1, Manu Chaudhary, Vivek Kumar Dwivedi
1Intellectual Scientific Division, Venus Medicine Research Center, Hill Top Industrial Estate, Bhatoli Kalan, Baddi, H.P. - 173205 India.
Abstract:
Drug toxicity is a common cause of liver injury and kidney failure. This study was designed to elucidate whether administration of high doses of Ceftriaxone or Vancomycin induce oxidative stress in liver as well as kidney, and to investigate the protective effects of VRP 1020 with fixed dose combination of ceftriaxone-vancomycin (Immunox-V). Twenty four Mus musculus mice (weighing 30 +/- 5 g) were divided into four groups containing six mice in each group. The activities of antioxidant enzymes such as superoxide dismutase, catalase and the level of malonaldialdehyde, as an marker of lipid per oxidation, were measured to evaluate oxidative stress in homogenates of the liver and renal tissue. Ceftriaxone or vancomycin administration significantly increased malonaldialdehyde levels (p < 0.001) but significant decreased in superoxide dismutase (p<0.01) and catalase (p<0.001) activities. Co-administration of VRP 1020 with FDC of Immunox-V injections caused significantly decreased malonaldialdehyde levels (p< 0.001) and increased superoxide dismutase (p<0.01) and catalase (p<0.001) activities in liver and renal tissue when compared with other treated groups. Similarly, the levels of extracellular antioxidant (Creatinine and Uric acid) were found to be significant lowered in Immunox-V treated group when compared to ceftriaxone or vancomycin alone treated group. These results indicate that chemical mediated technology of VRP 1020 with fixed dose combination of Immunox-V can prevent drug induced nephrotoxicity and oxidative stress which protects liver injury as well as renal tissue damage by reducing reactive oxygen species which improve the activities of free radical scavenging enzymes.
Insights
High doses of Ceftriaxone or Vancomycin cause liver and kidney oxidative stress. VRP 1020 with Immunox-V protects against this drug-induced damage by reducing reactive oxygen species.
Area of Science:
- Pharmacology
- Toxicology
- Biochemistry
Background:
- Drug-induced toxicity, particularly affecting the liver and kidneys, is a significant clinical concern.
- Ceftriaxone and Vancomycin are commonly used antibiotics with potential for causing organ damage.
- Oxidative stress plays a critical role in the pathogenesis of drug-induced organ injury.
Purpose of the Study:
- To investigate if high doses of Ceftriaxone or Vancomycin induce oxidative stress in the liver and kidneys.
- To evaluate the protective effects of VRP 1020, a fixed-dose combination of ceftriaxone-vancomycin (Immunox-V), against drug-induced oxidative stress.
- To assess the impact on antioxidant enzyme activities and lipid peroxidation markers.
Main Methods:
- Mice were divided into four groups and administered Ceftriaxone, Vancomycin, VRP 1020 with Immunox-V, or a control.
- Liver and kidney tissues were analyzed for malondialdehyde (MDA) levels as a marker of lipid peroxidation.
- Activities of antioxidant enzymes, including superoxide dismutase (SOD) and catalase, were measured.
- Levels of extracellular antioxidants, creatinine, and uric acid were assessed.
Main Results:
- Ceftriaxone or Vancomycin administration significantly increased MDA levels and decreased SOD and catalase activities.
- Co-administration of VRP 1020 with Immunox-V significantly reduced MDA levels and restored SOD and catalase activities in liver and kidney tissues.
- The Immunox-V group showed significantly lower levels of creatinine and uric acid compared to groups receiving Ceftriaxone or Vancomycin alone.
Conclusions:
- High-dose Ceftriaxone and Vancomycin induce significant oxidative stress in the liver and kidneys.
- VRP 1020, in combination with Immunox-V, demonstrates a protective effect against drug-induced nephrotoxicity and hepatotoxicity.
- This protective mechanism involves reducing reactive oxygen species and enhancing the activity of free radical scavenging enzymes.
