Riluzole and ranolazine application of prostate cancer: Cancer related testicular and liver tissue damage

Aim: In this study, utilizing the in vivo Copenhagen rat model possessing prostate cancer, we studied the possible impact of tumorigenesis on testes and liver morphology and whether riluzole (RIL) and ranolazine (RNL) treatment would have any affect or not. Method: Male Copenhagen rats were divided into four groups: 1) Control group, 2) Cancer group, 3) Cancer + 10 µM Riluzole 4), and Cancer + 2.5 µM / 5 µM Ranolazine group. The tissue samples of testes and liver were taken and processed for light microscopy, including staining with hematoxylin and eosin. Results: In the cancer group, degenerated seminiferous tubules, cell remnants in the lumen were shown in the testis, and a decrease in the spermatogenic cell line was found. The deterioration in these parameters was milder in the treatment groups and an increase in the number of normal tubules was found. In the cancer group, pyknotic nucleus, mononuclear cell infiltration, hyperemia, vacuolization, disrupted arrangement of hepatocyte plates, sinusoidal dilatations, and degenerated hepatocytes were observed in the liver. However, there was a slight damage in cancer + 10 µM RIL, cancer + 2.5 µM RNL, and cancer + 5 µM RNL groups. Properly hepatocyte arrangement and sinusoidal enlargement were observed. Conclusions: This treatment can be considered a promising protective adjuvant candidate for testes and liver tissue in prostate cancer or cancer therapy-related damage. &nbsp

Riluzole and ranolazine application of prostate cancer: Cancer related testicular andliver tissue damage

Aim: In this study, utilizing the in vivo Copenhagen rat model possessing prostate cancer, we studied the possible impact of tumorigenesis on testes and liver morphology and whether riluzole (RIL) and ranolazine (RNL) treatment would have any affect or not. Method: Male Copenhagen rats were divided into four groups: 1) Control group, 2) Cancer group, 3) Cancer + 10 μM Riluzole 4), and Cancer + 2.5 μM / 5 μM Ranolazine group. The tissue samples of testes and liver were taken and processed for light microscopy, including staining with hematoxylin and eosin. Results: In the cancer group, degenerated seminiferous tubules, cell remnants in the lumen were shown in the testis, and a decrease in the spermatogenic cell line was found. The deterioration in these parameters was milder in the treatment groups and an increase in the number of normal tubules was found. In the cancer group, pyknotic nucleus, mononuclear cell infiltration, hyperemia, vacuolization, disrupted arrangement of hepatocyte plates, sinusoidal dilatations, and degenerated hepatocytes were observed in the liver. However, there was a slight damage in cancer + 10 μM RIL, cancer + 2.5 μM RNL, and cancer + 5 μM RNL groups. Properly hepatocyte arrangement and sinusoidal enlargement were observed. Conclusions: This treatment can be considered a promising protective adjuvant candidate for testes and liver tissue in prostate cancer or cancer therapy-related damage

Gabapentin, an Analgesic Used Against Cancer-Associated Neuropathic Pain: Effects on Prostate Cancer Progression in an In Vivo Rat Model

A major problem associated with clinical management of cancer is controlling the accompanying pain, and various analgesics are in common use for this purpose. Recent evidence suggests that some of the targets of analgesics, such as ion channels and receptors, may also be involved in the cancer process, thereby raising the possibility that such use of some analgesics may impact upon cancer itself. The main aim of this study was to determine whether gabapentin, a common adjuvant analgesic in current use against cancer-associated neuropathic pain, would affect tumour development and progression in vivo. The Dunning rat model of prostate cancer was used. Strongly metastatic Mat-LyLu cells were implanted subcutaneously into syngeneic Copenhagen rats which were then treated every other day with 4.6-16.8 g/kg gabapentin by gavage. Primary tumourigenesis was monitored daily. Lung metastases were counted and measured after killing the rats 21 days later. Gabapentin had no effect on primary tumourigenesis but produced dose-dependent effects on lung metastasis. Whilst 4.6 g/kg had no effect, 9.1 g/kg gabapentin decreased the number of lung metastases significantly by 64%. In contrast, 16.8 g/kg gabapentin promoted metastasis significantly by 112% and showed a strong tendency to shorten mean survival time. It is concluded that gabapentin prescribed to cancer patients against pain could impact upon the cancer process itself