Investigation of serum enzyme activities and oxidative stress markers in preeclampsia: a multiparameter analysis.

OBJECTIVES: Preeclampsia, a high cause of fetomaternal morbidity-mortality, remains a significant burden affecting 8% of all pregnancies. Environmental conditions induce disease development leading to endothelial dysfunction in genetically predisposed women. Our aim is to discuss oxidative stress as a well-established contributing factor to disease progression with being the first study to show new evidence about serum dehydrogenase enzyme levels (isocitrate, malate, glutamate dehydrogenase) with oxidative markers (myeloperoxidase, total antioxidant-oxidant status, oxidative stress index). MATERIAL AND METHODS: Serum parameters were analyzed with photometric method (Abbott ARCHITECT c8000). RESULTS: The enzyme levels and oxidative markers were significantly higher in patients, supporting the redox imbalance in preeclampsia. According to ROC analysis, malate dehydrogenase showed an outstanding diagnostic ability with the highest AUC value of 0.9 and the cut-off value of 51.2 IU/L. Discriminant analysis including malate, isocitrate and glutamate dehydrogenase had predicted preeclampsia with an overall 87.9% accuracy. CONCLUSIONS: Considering the above results, we propose that the enzyme levels increase with oxidative stress functioning as antioxidant defense factors. The unique finding of the study is that the serum levels of malate, isocitrate and glutamate dehydrogenase can be used both separately and combined in the early prediction of preeclampsia. As a novel approach, we also offer combining serum isocitrate and glutamate dehydrogenase levels with ALT, AST tests to state liver functions more reliably in patients. Still, larger sample-sized studies investigating enzyme expression levels are required to confirm the recent findings and to reveal underlying mechanisms.

Effect of Camellia sinensis, Hypericum perforatum and Urtica dioica on kidney and liver injury induced by carbon tetrachloride in rats.

This study is aimed to investigate the effects of Camellia sinensis (CS), Hypericum perforatum (HP) and Urtica dioica (UD) in kidney and liver injury induced by carbon tetrachloride (CCl4) in rats. Highly toxic CCl4 which is used as a solvent in industry comprises experimental toxicity in rats and is widely used in hepatotoxicity and other tissue injury models. The purpose of this investigation is to monitor blood and various tissues by biochemical and histopathological analysis for preventive effects of CS, HP and UD on oxidative stress induced by administration of CCl4 and to enlighten the probable mechanism. Fifty eight rats were divided into five groups; sham group (Group 1, untreated animals), control CCl4 treated group (Group 2), HP extract-treated group (Group 3), UD extract-treated group (Group 4), CS extract-treated group (Group 5). All rats were anaesthetized at the end of the experiment and the blood was collected from each rat. Afterwards, tissue specimens were obtained. The tissue specimens were immersed in 10% formaldehyde for 24 hours. After routine tissue processing, the liver, kidney and stomach were sectioned in 5µm thickness, stained in hematoxylin and eosin. The histological study was performed by using light microscope. The serum marker enzymes were found to be significantly increased in CCl4-induced liver and kidney damage when compared with the sham group (p<0.05). However, treatment with CS, HP, and UD extracts resulted in decreased activity of serum enzymes. Malondialdehyde (MDA) levels were decreased by 20.51±0.95, 27.98±1.58, and 32.39±3.1 nmol/g wet weight protein in kidney homogenates and 16.65±1.75, 17.22±0.71 and 18.92±71 nmol/g wet weight protein in liver homogenates in CS, HP and UD treated groups, respectively. Our results have shown that additive antioxidants like CS, HP and UD will aid in diminishing these deviations in cases of liver and kidney dysfunction.

Assessment of Auditory Pathways Using Diffusion Tensor Imaging in Patients with Neurofibromatosis Type 1.

AIM: The aim of our study was to determine whether the diffusion properties of the auditory pathways alter between patients with Neurofibromatosis type 1 (NF1) and the healthy subjects. DTI can well demonstrate FA and ADC changes in auditory tracts and it may be a guide to identify the candidates for hearing loss among NF1 children. METHODS: The study population consisted of 43 patients with NF1 and 21 healthy controls. Diffusion tensor imaging (DTI) was used to measure apparent diffusion coefficient (ADC) and fractional anisotropy (FA) values from lemniscus lateralis, colliculus inferior, corpus geniculatum mediale and Heschl's gyrus. The results were compared with those of the control group. RESULTS: The ADC values of lateral lemniscus, colliculus inferior and corpus geniculatum mediale were significantly higher in NF1 compared to those of the control group. On the other hand, decreased FA values were observed in lateral lemniscus and colliculus inferior in patients with NF1. CONCLUSION: The increase in ADC and reduction in FA in the auditory pathways of patients with NF1 may suggest microstructural alterations, such as a decrease in the number of axons, edema or inflammation in the auditory tracts.

The protective effects of caffeic acid phenethyl ester against toluene-induced nephrotoxicity in rats.

Caffeic acid phenethyl ester (CAPE) has antioxidant and anti-inflammatory properties. The aim of this study is to examine the negative effects of toluene on kidney tissues and functions and to investigate the protective effects of CAPE against toluene-induced nephrotoxicity in rats. A total of 21 male Wistar rats were divided into three groups of equal number in each. The rats in group I were the controls. Toluene was intraperitoneally injected into the rats in group II with a dose of 500 mg/kg. Rats in group III received CAPE daily while exposed to toluene. After 14 days of experimental period, all rats were killed by decapitation. Enzymatic activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) and malondialdehyde (MDA) levels were studied in the rat kidneys. Blood urea nitrogen (BUN) and serum creatinine levels were measured for renal function. The CAT and SOD enzyme activities and serum creatinine levels were significantly increased in rats treated with toluene when compared with the controls. But GSH-Px activity, MDA, and BUN levels showed statistically nonsignificant changes. However, increased CAT and SOD enzyme activities and decreased serum creatinine levels were detected in the rats that received CAPE while exposed to toluene. The GSH-Px activity and MDA and BUN levels in the same group did not show statistically significant changes. The results of our study demonstrated that toluene damages kidney tissue and is a nephrotoxic substance. CAPE was able to prevent the renal damage as antioxidant, antitoxic, and nephroprotective agent.

Protective effects of omega-3 essential fatty acids against formaldehyde-induced cerebellar damage in rats.

This study aimed to investigate changes in the cerebellum of formaldehyde-exposed rats and the effects of omega-3 fatty acids on these changes. The study involved 21 male Wistar-Albino rats which were divided into three groups. The rats in Group I comprised the control group. The rats in Group II were injected with intraperitoneal 10% formaldehyde every other day. The rats in Group III received omega-3 fatty acids daily while exposed to formaldehyde. At the end of the 14-day experimental period, all rats were killed by decapitation and the cerebellum removed. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), xanthine oxidase (XO), and malondialdehyde (MDA) levels were determined in cerebellum specimens by using spectrophotometric methods. In our study, levels of SOD and CAT were significantly decreased, and GSH-Px, XO, MDA levels were significantly increased in rats treated with formaldehyde compared with those of the controls. Whereas, it was seen that there was an increase in SOD and CAT enzyme activities and decrease in MDA, XO, and GSH-Px levels in rats administered to omega-3 fatty acids with exposure of formaldehyde. It was determined that exposure of formaldehyde increased free radicals in cerebellum of rats and this increase was prevented by administration of omega-3 fatty acids.

Hepatotoxic activity of toluene inhalation and protective role of melatonin.

This study was designed to investigate the harmful effects of toluene inhalation in the liver of rats and possible protective effects of melatonin on these detrimental effects. For this purpose, 21 adult male Wistar-albino rats were randomly divided into three equal groups. Animals in group I were used as control. The rats in group II were exposed to toluene (3000 ppm/1 hour/day) for 4 weeks, while the rats in group III were treated with melatonin (10 mg/kg/day, intraperitoneally [ip]) plus toluene inhalation. At the end of the experimental period, liver and blood samples were taken from the decapitated animals. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin and albumin levels were determined. Liver tissue sections were stained with routine histological methods and examined under the light microscope. In addition, the sections were immunohistochemically stained using avidin-biotin-peroxidase method for determination of apoptosis. The liver tissue activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and malondialdehyde (MDA) levels were also measured. Toluene inhalation significantly increased serum ALT, AST and tissue MDA, and decreased serum albumin, but did not affect serum ALP, total bilirubin levels and tissue SOD, GSH-Px and CAT activity when compared with controls. The increases in tissue MDA and serum ALT and AST levels induced by toluene inhalation were significantly inhibited by melatonin treatment. In light microscopic observations of tissues from toluene-inhaled rats, massive hepatocyte degeneration, ballooning degeneration and mild pericentral fibrosis were observed. Bax immune reactivity was also increased significantly. Melatonin treatment decreased the balloon degeneration, fibrosis and Bax immune reactivity in the liver of toluene-inhaled rats. In view of the present findings, it is suggested that melatonin has hepatoprotective effects against toluene toxicity via primarily antioxidative properties.

Salt and nitric oxide synthase inhibition-induced hypertension: kidney dysfunction and brain anti-oxidant capacity.

The specific aim of this study was to examine the effects of salt-loading on kidney function and brain antioxidant capacity. Wistar rats were divided into four groups: Control rats were given normal drinking water and no drug treatment for 2 weeks. LNNA group: rats were given normal drinking water and the nitric oxide (NO) inhibitor NG-nitro-L-arginine (L-NNA), 3 mg/kg/day. LNNA + Salt group: rats were given drinking water containing salt 2% and 3 mg/kg L-NNA. Salt group: rats were given drinking water containing salt 2% and no drug treatment. Basal blood pressure and the levels of serum BUN, creatinine, uric acid, cortisol, electrolyte, serum antioxidant capacity, and oxidative stress were measured. NO, superoxide dismutase (SOD), and catalase (CAT) levels were measured in the hypothalamus, brainstem, and cerebellum. Salt overload increased the blood pressure of the LNNA + Salt group. Salt-loading enhanced BUN, creatinine, sodium retention. High salt produced an increase in uric acid levels and a decrease in cortisol levels in serum. Additionally, the oxidative stress index in serum increased in the LNNA + Salt group. Salt-loading enhanced brain NO levels, but not SOD and CAT activity. L-NNA increased brain SOD activity, but not CAT and NO levels. In conclusion, salt-loading causes hypertension, kidney dysfunction, and enhances oxidative stress in salt-sensitive rats.

Effects of testosterone on orchiectomy-induced oxidative damage in the rat hippocampus.

The aim of this study was to investigate the morphological changes of the hippocampus after orchiectomy and the protective effects of testosterone on these changes. Animals were divided into 3 groups. The rats in group I were used for sham-orchiectomy. Orchiectomy was performed on the rats in group II. The rats in group III were administrated testosterone propionate 0.5mg/kg/day for 30 days after the orchiectomy. Some of the hippocampal tissues were used for determination of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) enzyme activities, and malondialdehyde (MDA) levels. The remaining hippocampal tissue specimens were stained with routine histological methods and examined under the light microscope. Additionally, the samples were immunohistochemically stained by using avidin-biotin-peroxidase for determination of bax immunoreactivity. The SOD and GSH-Px enzyme activities of the hippocampus were decreased, and MDA levels were increased in group II rats compared to the sham-orchiectomy group. In the light microscopic evaluation of the tissue specimens from group II, significant increases were detected in the number of picnotic cells and in bax immunoreactivity compared to the sham-orchiectomy group. However, an increase was observed in activities of SOD and GSH-Px enzymes and a decrease of the MDA levels in animals with orchiectomy, but having externally administered testosterone. It was determined that the increase of bax immunoreactivity and histopathological changes in this group were regressed by testosterone. The results of our study revealed that orchiectomy-induced oxidative damage and morphological changes in the hippocampal tissue were suppressed by testosterone.

Beneficial effect of erdosteine on methotrexate-induced testicular toxicity in mice.

Methotrexate is used to treat certain types of cancer of the breast, skin, head and neck, or lung. Methotrexate can cause serious or life-threatening side effects on liver, lungs, kidneys, and immune system. Methotrexate chemotherapy causes testicular damage in humans. The aim of this study was to investigate the possible protective role of erdosteine on testicular toxicity of methotrexate in mice. Twenty-six male mice were divided into four groups as follows: group 1, control; group 2, erdosteine-treated; group 3, methotrexate-treated; and group 4, methotrexate + erdosteine treated. On the first day of experiment, a single dose of methotrexate was intraperitoneally administered to groups 3 and 4, although a daily single dose of erdosteine was orally administered to group 2 and 4 for 7 days. At the end of the experiment, the testes of the animals were removed and weighed. The levels of total antioxidant capacity and total oxidative stress, and myeloperoxidase activity in the methotrexate group were higher than the control group (p<0.05). Lipid peroxidation levels were not changed in methotrexate group compared with control group. In conclusion, erdosteine could effectively protect the testes in methotrexate-induced toxicity.

Melatonin prevents formaldehyde-induced neurotoxicity in prefrontal cortex of rats: an immunohistochemical and biochemical study.

This study was undertaken to investigate the protective effects of melatonin against formaldehyde-induced neurotoxicity in prefrontal cortex of rats. For this purpose, 21 male Wistar rats were divided into three groups. The rats in Group I were used as a control, while the rats in Group II were injected every other day with formaldehyde. The rats in Group III received melatonin daily while exposed to formaldehyde. At the end of 14-day experimental period, all rats were killed by decapitation. The brains of the rats were removed and the prefrontal cortex tissues were obtained from all brain specimens. Some of the prefrontal cortex tissue specimens were used for determination of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) levels. The remaining prefrontal cortex tissue specimens were used for immunohistochemical evaluation. The levels of SOD and GSH-Px were significantly decreased, and MDA levels, were significantly increased in rats treated with formaldehyde compared with those of the controls. In the immunohistochemical evaluation of this group, apoptotic cells were observed. However, increased SOD and GSH-Px enzyme activities, and decreased MDA levels, were detected in the rats administered melatonin while exposed to formaldehyde. Furthermore, apoptotic changes caused by formaldehyde were decreased in these rats. The results of our study suggest that melatonin treatment prevents formaldehyde-induced neuronal damage in prefrontal cortex.