IntroductionChemotherapy drugs are used in the treatment of various types of cancers. Their toxicities and minor risks are often overlooked as a result of their potential usefulness in treatment. In particular, testicular cells have been selected as targets by chemotherapeutic agents, as they enter various mitotic, meiotic, and morphological processes and therefore they are easily damaged [1]. Cis-diamminedichloroplatinum (II) or cisplatin (CP), a highly effective antineoplastic DNA alkylating agent, has been used to treat a wide variety of solid tumors, such as those in the testicles, ovaries, breast, lungs, bladder, head, and neck [2]. However, the use of the drug is limited due to side effects, such as testicular toxicity, cachexia, and testicular damage [2,3]. When CP is administered at a high cumulative dose, it can result in permanent azoospermia and then infertility in patients [3]. CP interacts with DNA to create cross-link and intra-chain cross-links. Since the DNA modified by CP cannot be sufficiently renewed, the DNA damage initiates apoptosis [4].Caffeic acid phenethyl ester (CAPE) is one of the active ingredients of the sharp and fragrant propolis substance found in the extract collected by bees from plants. CAPE has been used as a folk remedy for many years [5]. Antimicrobial, antiinflammatory, immunomodulatory, antimutagenic, antioxidant, and anticarcinogenic effects of propolis have been demonstrated by various studies. CAPE, one of the active ingredients of propolis, and has an important place in these beneficial effects [6,7]. Although CAPE is a pharmacologically safe compound, it also reduces lipid peroxidation and stimulates antioxidant enzyme activity [8].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 µmol/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 µmol/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 come...
Chronic hypoxia negatively affects male fertility by causing pathological changes in male reproductive system. However, underlying mechanisms of this damage are unknown. Chloroquine (CLQ) is an anti‐inflammatory agent that is widely used in the treatment of inflammation‐related diseases such as malaria and rheumatoid arthritis. This study aimed to investigate the therapeutic effects of CLQ in the hypoxia‐induced testicular damage via assessment of hypoxic response, endoplasmic reticulum stress and apoptosis. For this purpose, 32 Wistar albino rats were divided into 4 groups as control (given 20%‐21% O2, no treatment), CLQ (given 50 mg/kg and 20%‐21% O2 for 28 days), hypoxia (HX) (given 10% O2 for 28 days) and HX + CLQ (given 50 mg/kg and 10% O2 for 28 days). After the experiment, blood samples and testicular tissues were taken. Histopathological evaluation was performed on testicular tissues and hypoxia‐inducible factor 1‐α (HIF1‐α), heat shock proteins (HSPs) HSP70, HSP90 and growth arrest and DNA damage‐inducible gene 153 (GADD153) expression levels were detected via immunohistochemistry. Moreover, apoptotic cells were detected via terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining and serum testosterone levels were determined by enzyme‐linked immunosorbent assay (ELISA) assay. Histopathological changes, apoptotic cell numbers and HIF1‐α, HSP70, HSP90 and GADD153 expressions significantly increased in HX group (P < .05). Moreover, serum testosterone levels decreased in this group (P > .05). However, CLQ exerted a strong ameliorative effect on all parameters in HX + CLQ group. According to our results, we suggested that CLQ can be considered as an alternative protective agent for eliminating the negative effects of hypoxic conditions on male fertility.
In this study, we aimed to determine the effects of autophagy inhibitor and activator on Cisplatin (Cis)induced tissue damage. Materials and Methods: A total of 24 male Wistar albino rats were divided into 4 groups including 6 rats per group in this study. Groups are as follows; Control, Cisplatin (Cis) (8 mg/kg), Rapamycin (Rapa) (2 mg/kg), 3methyladenine (3-MA) (15 mg/kg). Rapa and 3-MA were given intraperitoneally for 15 days. Cis was administered as a single dose on the 7th day of the experimental period. At the end of the experimental procedure, epididymis tissues were extracted. Hematoxylin and eosin staining and Heat shock protein-70 (HSP70) immunohistochemistry were applied to the sections taken after histological techniques. Results: Dispersion in the tubule basement membrane and vacuolization in the tubule was observed in the Cis group. It was also observed that some epithelial cells were more eosinophilic in the Cis group. Tissue sections of Rapa and 3-MA had a more regular appearance in terms of epithelization and tubule basement membrane. HSP70 immunoreactivity was observed in the intertubuler connective tissue of all groups. Conclusion:The epididymis was affected by agents such as Cis in terms of the protection of semen quality and potency of spermatozoa. Rapa may be more effective than 3-MA in the epididymis against Cis toxicity. Amaç: Bu çalışmada sisplatin (Cis) doku üzerinde neden olduğu hasar üzerinde otofaji aktivatörü ve inhibitörü etkilerinin belirlenmesi amaçlanmıştır. Gereç ve Yöntem: Çalışmada her grupta 6 hayvan olacak şekilde 24 adet Wistar albino cinsi erkek sıçan kullanıldı. Gruplar; Kontrol grubu, Sisplatin grubu (Cis) (8 mg/kg), Rapamisin (Rapa) grubu (2 mg/kg), 3-metiladenin grubu (3-MA) (15 mg/kg). Rapa ve 3-MA intraperitoneal 15 gün boyunca, Cis tek doz deneyin 7. Günü uygulandı. Deney sonunda epididimisler alındı. Histolojik teknikler sonrası alınan kesitlere Hematoksilen-Eozin ve Heat-shock-protein70 (HSP70) immunohistokimyası uygulandı. Bulgular: Cis kesitlerinde tübül bazal membranında dağılma, tübül içinde vakuolizasyon gözlendi. Ayrıca bazı epitel hücrelerinin daha eozinofilik olduğu gözlendi. Rapa ve 3-MA ait doku kesitleri epitelizasyon, tübül bazal membranı olarak daha düzenli bir görünüme sahipti. HSP70 immunreaktivitesi tüm grupların tübüler arası bağ dokusunda gözlendi. Sonuç: Semen kalitesi ve spermatozoanın potansiyelliğinin korunması için organın Cis gibi ajanlardan etkilendiği sonucuna varılmıştır. Rapa, Cis toksisitesine karşı epididimis üzerinde 3-MA'den daha etkili olabilir.
Purpose. To determine the protective effects of melatonin (MEL) in acute kidney injury (AKI) induced by Cisplatin (CP), widely used as a chemotherapeutic in the treatment of many cancer types, via assessment of heat-shock proteins (HSPs) levels in rats. Methods. Total 40 Wistar albino rats were divided into four groups: Control (n = 10), MEL (n = 10, 10 mg/kg/i.p melatonin for 8 days), CP (n = 10, 7 mg/kg/i.p cisplatin at the 5th day), and CP + MEL (n = 10, 10 mg/kg/i.p melatonin for 8 days and 7 mg/kg/i.p cisplatin at the 5th day). After administrations, animals were sacrificed, and kidney tissues were extracted. Histopathological changes were evaluated and glomerular and tubular immunoreactivities of HSP47, HSP60, HSP7, and HSP90 in renal cortex were detected by immunohistochemistry. Moreover, blood serum BUN, creatinine and uric acid levels were measured to assess of kidney function. Results. CP group showed histopathological deterioration compared to Control group and MEL treatment attenuated this damage. When compared with Control and MEL groups, an increase in HSPs immunoreactivities in renal cortex and blood serum BUN, creatinine and uric acid levels were observed in the CP group. Furthermore, an improvement was observed in the CP + MEL in terms of these parameters compared to the CP group. Conclusion. According to our results, MEL could exert a significant protective effect to ameliorate CP-induced AKI via regulation of heat-shock protein expressions.
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.
Diabetes mellitus associated with oxidative stress and inflammation can affect many organs. While the effects of diabetes on many organs are well known and documented, its mechanisms of action on the lung are known far less. Hyperglycemia can lead to lung damage by increasing oxidative stresses and inflammation. Diabetes may be a trigger for pulmonary fibrosis, as studies suggest that there may be an important link between pulmonary fibrosis and diabetes. In this review, the histopathological changes caused by diabetes in the lung tissue were summarized. In addition, changes in the lung due to inflammation, oxidative stress and pulmonary fibrosis mechanisms were evaluated.
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