ABSTRACT
OBJECTIVE: The aim of this study is to investigate the possible protective effects of melatonin and caffeic acid phenethyl ester (CAPE) on potassium dichromate (K2 Cr2O7)-induced nephrotoxicity and genotoxicity. METHODS: A total of 40 Wistar albino rats were divided into five groups: control, K2Cr2O7(K2Cr2O715 mg/kg, one dose, i.p.), K2Cr2O7 + melatonin, K2Cr2O7 + CAPE, and K2Cr2O7 + melatonin + CAPE. Urine and blood samples were collected from rats before scarification. One kidney was collected for histopathological studies, and the other was stored at -80°C for further determination of catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), glutathione S-transferase (GST), and glutathione reductase (GR) levels with spectrophotometric method. Comet assay was used to evaluate the genotoxicity. RESULTS: We observed a significant amelioration in genotoxicity by melatonin and simultaneous melatonin + CAPE treatment compared to K2Cr2O7 group (p1, p2< 0.05). SOD, CAT, GSH, GST, and MDA levels did not change when compared with controls. When K2Cr2O7 applied group was treated with melatonin and CAPE, neither melatonin nor CAPE made any changes in kidney GSH, GST, SOD, and MDA levels (P > 0.05). We noted that treatment with CAPE and melatonin + CAPE together caused a significant decrease in renal tissue damage, an upregulation in the kidney CAT levels (P < 0.05) and a slight healing at GR levels when compared with the K2Cr2O7 group. CONCLUSION: Our results revealed, CAPE and melatonin may have protective effects on K2Cr2O7 induced nephrotoxicity and cellular damage in rats.
Subject(s)
Acute Kidney Injury/drug therapy , Caffeic Acids/therapeutic use , DNA Damage/drug effects , Kidney/drug effects , Melatonin/therapeutic use , Phenylethyl Alcohol/analogs & derivatives , Potassium Dichromate/toxicity , Animals , Caffeic Acids/administration & dosage , Comet Assay , Drug Therapy, Combination , Enzyme-Linked Immunosorbent Assay , Kidney/enzymology , Kidney/pathology , Kidney Function Tests , Melatonin/administration & dosage , Melatonin/blood , Oxidative Stress/drug effects , Phenylethyl Alcohol/administration & dosage , Phenylethyl Alcohol/therapeutic use , Rats, WistarABSTRACT
OBJECTIVE: Panic disorder (PD) is an anxiety disorder characterized by sudden attacks of intense fear. Biochemical studies suggest that oxidative stress (OS) index is significantly higher in PD, and OS genes may participate in development of anxiety-like behavioral phenotypes. We aimed to investigate role of polymorphisms in OS gene, glutathione peroxidase-1 (GPX1), and DNA repair enzyme gene, 8-oxoguanine glycosylase-1 (OGG1), in PD patients. METHODS: GPX1 Pro198Leu (rs1050450) and OGG1 Ser326Cys (rs1052133) polymorphisms of 127 patients with PD and 151 disease-free controls were analyzed with real-time polymerase chain reaction. Severity of PD symptoms was assessed by Panic and Agoraphobia Scale (PAS). RESULTS: No significant relationship was found in genotype distributions of OGG1 Ser326Cys and GPX1 Pro198Leu polymorphisms between PD and control groups (p > 0.05). There was no significant relationship between OGG1 or GPX1 polymorphisms, and age of onset, agoraphobia, or PAS scores in PD group (p > 0.05). However, in GPX1 Pro198Leu polymorphism, C allele (Pro) was found to be more frequent in female subgroup of PD patients compared with that in males (p = 0.027). CONCLUSIONS: GPX1 Pro198Leu and OGG1 Ser326Cys polymorphisms were not associated with PD risk in Turkish patients. However, a gender-specific effect of GPX1 Pro198Leu C allele may be associated with PD development.
