Although radiation is one of the basic methods commonly used in cancer treatment, it inevitably enters the field of treatment in healthy tissues and is adversely affected by the acute and chronic s...

Background/aim: Cisplatin (CP), a chemotherapeutic drug, causes damage to spermatogenic serial cells, Sertoli cells, and Leydig cells in rat testicles. It was aimed to investigate the protective effect of caffeic acid phenethyl ester (CAPE), one of the active ingredients of propolis, in eliminating CP-induced testicular damage. Materials and methods: Group 1 (control group) was given physiological saline solution intraperitoneally (IP) throughout the experiment. Group 2 (CP group) was given a single dose of CP (7 mg/kg) IP on the day 7. Group 3 (CP + CAPE group), was given CAPE (10 mu mol/kg/day) IP for 12 days and a single dose of CP (7 mg/kg) IP on day 7. Group 4 (CAPE group) was given CAPE (10 mu mol/kg/day) IP for 12 days. On day 14 of the experiment, the rats were decapitated under xylazine and ketamine anesthesia and their testicles were removed. The sections obtained from the testicles were stained with hematoxylin-eosin and histopathological damage was evaluated. Malondialdehyde (MDA) levels, and superoxide dismutase (SOD) and catalase (CAT) enzymatic activities were measured in the testicular tissue samples. Testosterone (TES) levels were measured in the blood serum. The Johnsen testicular biopsy score (JTBS) was used to evaluate testicular tubules. DNA damage was evaluated in sperm samples taken from the ductus epididymis using the comet assay technique. Results: In Group 2, which was given CP, the testicles were severely damaged. It was observed that histological damage was reduced in the testes by administering CAPE in Group 3. Moreover, according to the TITS, the value was significantly higher in the testicular tubules (P < 0.05). Moreover, the MDA level decreased in Group 3. However, the SOI), CAT, and TES levels increased in Group 3. DNA damage also decreased significantly in Group 3 when compared to Group 2 (P < 0.05). Conclusion: The results showed that CAPE may be protective against damage caused by CP in the testicles of rats.

Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti‐inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin–eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), Cas‐3, and nerve growth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas‐3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis‐associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure.

Background/aim: Paclitaxel is a widely used drug for the treatment of cancer, but it possesses toxic effects on male reproductive system. Administering paclitaxel with an antioxidant has become a strategy for preventing the side effects of paclitaxel. Although curcumin is an antioxidant, data concerning the effect of curcumin on paclitaxel-induced testis tissue are lacking. The present study was established to examine the protective impact of curcumin against testicular damage induced by paclitaxel. Materials and methods: In the study, 40 Wistar albino male rats were used and randomly divided into 4 groups (n:10). The control group received only saline solution; the curcumin group received curcumin throughout the experiment; the paclitaxel group received a total of four doses of paclitaxel on days 1, 7, 14, and 21 of the experiment; curcumin + paclitaxel group received curcumin throughout the experiment and a total of four doses of paclitaxel on days 1, 7, 14, and 21 of the experiment. At the end of the experiment, the rats were decapitated under xylazine and ketamine anesthesia and their testicles were removed. The sections obtained from the testicles were stained with Hematoxylin & Eosin and histopathological damage was evaluated. The TUNEL method was applied to determine apoptotic cells. Testosterone levels were measured in the blood serum. The Johnsen testicular biopsy score (JTBS) was used to evaluate testicular tubules. DNA damage was evaluated in sperm samples taken from the ductus epididymis using the comet assay technique. Results: Testicular tissue was severely damaged in the paclitaxel group. In the curcumin + paclitaxel group, it was determined that the administration of curcumin with paclitaxel reduced the histological damage in the testicular tissue. Moreover, according to the JTBS, the value was significantly higher in the testicular tubules (p < 0.05). Testosterone levels were higher in curcumin + paclitaxel group than in paclitaxel group. DNA damage also decreased significantly in curcumin + paclitaxel group when compared to paclitaxel group (p < 0.05). Conclusion: The results showed that curcumin may be protective against damage caused by paclitaxel in the testicles of rats.