article · Environmental Toxicology
Ehrlich ascites carcinoma induces significant renal toxicity and structural damage in mice, characterised by glomerular atrophy, DNA damage, and altered blood and kidney parameters. Investigating the protective properties of vitamin B17, female mice were evaluated across control, cancer, pretreatment, and cotreatment groups. Administering vitamin B17 either before or alongside the cancer model led to marked improvements in cytological health, reduced DNA damage, and restored kidney structure. The treatment significantly lowered elevated urea, creatinine, potassium, platelets, and white blood cell counts, while raising sodium, red blood cells, haemoglobin, and hematocrit levels. In addition, vitamin B17 intervention reduced renal P53 and proliferating cell nuclear antigen protein expression compared to the untreated cancer group. Pretreatment offered moderate histological improvements while cotreatment provided mild enhancement, demonstrating a protective effect against cancer-induced kidney injury.
Cancer progression and related systemic toxicity can cause severe kidney damage and metabolic disruptions. Demonstrating that vitamin B17 can alleviate renal injury, normalise critical blood parameters, and preserve kidney tissue architecture in experimental models highlights its potential role as a protective agent. This provides foundational insight for further exploration of supportive interventions to counter cancer-associated organ toxicities.
This research represents early-stage animal testing evaluating vitamin B17 as a nephroprotective agent against cancer-induced kidney injury. Potential applications could eventually include supportive therapeutic formulations or nutraceutical supplements aimed at mitigating organ damage during oncology management. However, the findings are currently restricted to preclinical mouse models, meaning practical use remains far from market and dependent on extensive clinical safety and efficacy studies.
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Cancer is the major cause of death and many factors that lead to its occurrences, such as environmental pollution and pesticides and other factors. Ehrlich carcinoma development depends on many things associated with the environment, nutrition, personal habits, and family history. The present study aimed to evaluate the potential protective effects of vitamin B17 (VB17) against Ehrlich ascites carcinoma (EAC) that induced kidney toxicity in female mice. The mice were divided into five groups (first group, control group; second group, VB17 group; third group, EAC group; fourth group, pretreated EAC with VB17; fifth group, cotreated EAC with VB17). Results showed the VB17 in pretreated (G4) and cotreated (G5) groups lead to an improvement in DNA damage and cytological examination, in addition significantly (P < .05) increase in Na<sup>+</sup> , red blood cell, hemoglobin, hematocrit value, mean corpuscular hemoglobin (MCH), and MCH concentration, whereas significantly (P < .05) decrease in urea, creatinine, K<sup>+</sup> , platelets, and white blood cells while insignificant (P < .05) changes in mean corpuscular volume when compared to the EAC group. Many histopathological changes were observed in kidney sections in EAC as marked damage and degenerated, glomerular atrophy, the Malpighian corpuscles that lost their characteristic configuration. On the other hand, a moderate improvement and arrangement in the kidney histological structure in pretreated VB17 + EAC, while a mild enhancement and arrangement of the kidney structure in cotreated EAC + VB17. In addition, depletion in renal P53 and PCNA protein expression compared with the EAC group. It could be concluded that VB17 has a potential renal protective effect against EAC cells induced kidney injury.
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DOI: 10.1002/tox.22888
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