Purpose: Clear cell renal cell carcinoma (ccRCC) is the most common histological subtype of renal carcinoma, accounting for 75%–80% of cases. Vascular endothelial growth factor (VEGF), which promotes angiogenesis via its membrane receptors (VEGFRs), and E-cadherin, which decreases in expression during invasion and metastasis, are both implicated in ccRCC pathogenesis. We analyzed the relationship between these proteins and ccRCC lesions to assess their usefulness as prognostic markers. Materials and Methods: Renal tumor tissue samples from nephrectomies of 69 patients were analyzed using immunohistochemical techniques to evaluate the expression of the aforementioned proteins. These findings were then compared with established prognostic scales. Statistical analysis was performed using SPSS Statistics ver. 29.0.1.0. Results: VEGF intensity was significantly correlated with tumor size (T; p=0.002), stage (p<0.001), and metastasis (M; p=0.049) according to the TNM classification. VEGFR3 expression correlated positively with tumor size (T; p=0.046) and stage (p=0.040). E-cadherin expression correlated negatively with tumor size (p=0.047). In relation to prognostic scales, VEGF expression correlated with the UCLA Integrated Staging System score (p=0.009), while E-cadherin correlated with the stage, size, grade and necrosis (SSIGN) score (p=0.044). For both overall and disease-free survival, significant differences were observed between the moderate (2++) and intense (3+++) VEGFR3 intensity groups (p=0.009 for both). Conclusion VEGF may have prognostic value due to its association with tumor size, stage, metastasis, and the UCLA Integrated Staging System score. Similarly, VEGFR3 shows prognostic potential based on its correlations with tumor size, stage, and its relation to overall and disease-free survival. E-cadherin also demonstrates prognostic significance through its association with tumor size and the SSIGN score.

Previous research on the well-known environmental pollutant fluoride has demonstrated that fluoride exposure can lead to oxidative stress-related male infertility. Obesity is another public health issue that has a detrimental impact on male fertility. Previously, findings on fluoride toxicity in high-fat diet (HFD) conditions associated with oxidative stress have been evidenced. This study aimed to evaluate the impact of subchronic fluoride exposure (5 mg/kg) plus a HFD on testicular alteration in Wistar rats. Animals were divided into four groups (control, HFD, fluoride, and fluoride 5 mg/kg plus HFD). The HFD contained a 50% kcal increase in fat (saturated fat), after 90 days of co-exposure to fluoride plus HFD, the animals showed a significant decrease in the adiposity index. The co-exposed group showed oxidative damage assessed through decreased glutathione (GSH) concentration (p < 0.0001), increased concentrations of malondialdehyde (MDA) (p < 0.0001), and the oxidation of proteins (p < 0.0001) vs the control group. Finally, testicular histology exhibited a reduction in spermatogonia and spermatocytes. The results of the study indicate that under these conditions, subchronic co-exposure to fluoride under HFD conditions could protect against the accumulation of epididymal fat, however, oxidative alteration at the testicular level is maintained.

Previous research on the well-known environmental pollutant fluoride has demonstrated that fluoride exposure can lead to oxidative stress-related male infertility. Obesity is another public health issue that has a detrimental impact on male fertility. Previously, findings on fluoride toxicity in high-fat diet (HFD) conditions associated with oxidative stress have been evidenced. This study aimed to evaluate the impact of subchronic fluoride exposure (5 mg/kg) plus a HFD on testicular alteration in Wistar rats. Animals were divided into four groups (control, HFD, fluoride, and fluoride 5 mg/kg plus HFD). The HFD contained a 50% kcal increase in fat (saturated fat), after 90 days of co-exposure to fluoride plus HFD, the animals showed a significant decrease in the adiposity index. The co-exposed group showed oxidative damage assessed through decreased glutathione (GSH) concentration (p < 0.0001), increased concentrations of malondialdehyde (MDA) (p < 0.0001), and the oxidation of proteins (p < 0.0001) vs the control group. Finally, testicular histology exhibited a reduction in spermatogonia and spermatocytes. The results of the study indicate that under these conditions, subchronic co-exposure to fluoride under HFD conditions could protect against the accumulation of epididymal fat, however, oxidative alteration at the testicular level is maintained.

Previous research on the well-known environmental pollutant fluoride has demonstrated that fluoride exposure can lead to oxidative stress-related male infertility. Obesity is another public health issue that has a detrimental impact on male fertility. Previously, findings on fluoride toxicity in high-fat diet (HFD) conditions associated with oxidative stress have been evidenced. This study aimed to evaluate the impact of subchronic fluoride exposure (5 mg/kg) plus a HFD on testicular alteration in Wistar rats. Animals were divided into four groups (control, HFD, fluoride, and fluoride 5 mg/kg plus HFD). The HFD contained a 50% kcal increase in fat (saturated fat), after 90 days of co-exposure to fluoride plus HFD, the animals showed a significant decrease in the adiposity index. The co-exposed group showed oxidative damage assessed through decreased glutathione (GSH) concentration (p < 0.0001), increased concentrations of malondialdehyde (MDA) (p < 0.0001), and the oxidation of proteins (p < 0.0001) vs the control group. Finally, testicular histology exhibited a reduction in spermatogonia and spermatocytes. The results of the study indicate that under these conditions, subchronic co-exposure to fluoride under HFD conditions could protect against the accumulation of epididymal fat, however, oxidative alteration at the testicular level is maintained.

Previous research on the well-known environmental pollutant fluoride has demonstrated that fluoride exposure can lead to oxidative stress-related male infertility. Obesity is another public health issue that has a detrimental impact on male fertility. Previously, findings on fluoride toxicity in high-fat diet (HFD) conditions associated with oxidative stress have been evidenced. This study aimed to evaluate the impact of subchronic fluoride exposure (5 mg/kg) plus a HFD on testicular alteration in Wistar rats. Animals were divided into four groups (control, HFD, fluoride, and fluoride 5 mg/kg plus HFD). The HFD contained a 50% kcal increase in fat (saturated fat), after 90 days of co-exposure to fluoride plus HFD, the animals showed a significant decrease in the adiposity index. The co-exposed group showed oxidative damage assessed through decreased glutathione (GSH) concentration (p < 0.0001), increased concentrations of malondialdehyde (MDA) (p < 0.0001), and the oxidation of proteins (p < 0.0001) vs the control group. Finally, testicular histology exhibited a reduction in spermatogonia and spermatocytes. The results of the study indicate that under these conditions, subchronic co-exposure to fluoride under HFD conditions could protect against the accumulation of epididymal fat, however, oxidative alteration at the testicular level is maintained.