microRNA profiling for early detection of nonmelanoma skin cancer.

BACKGROUND: microRNAs (miRNAs) are single-stranded, noncoding RNA molecules. Given the vast regulatory potential of miRNAs and their often tissue-specific and disease-specific expression patterns, miRNAs are being assessed as possible biomarkers to aid diagnosis and prediction of different types and stages of cancers, including skin cancer. Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are the most common forms of nonmelanoma skin cancer (NMSC). BCC originates from the basal layer of the epidermis, while SCC arises from epidermal keratinocytes or from the dermal appendages. Although NMSCs are currently the most common types of malignancies, both BCC and SCC have a better than 95% cure rate if detected early. AIM: To identify plasma miRNAs suitable for early detection of NMSC. METHODS: Expression profiles of 741 miRNAs were evaluated using high-throughput real-time quantitative PCR from plasma samples in 42 patients with NMSC and 282 healthy controls (HCs). RESULTS: Our results demonstrated that in patients with NMSC, compared with HCs, expression levels of miR-30e-3p, miR-145-5p, miR-186-5p and miR-875-5p were significantly (P < 0.05) upregulated, while those of miR-19a-3p, miR-25-3p, miR-30a-5p, miR-451 and miR-576-3p were significantly downregulated. CONCLUSION: Our study suggests that the miRNAs with significant changes in expression (miR-19a-3p, miR-25-3p, miR-30a-5p, miR-145-5p and miR-186-5p) could serve as novel noninvasive biomarkers for detection of NMSC.

Circulating microRNA expression profiles in ovarian cancer.

MicroRNA (miRNA) is an abundant class of small non-coding RNAs that act as gene regulators. Recent studies have suggested that miRNA deregulation is associated with the initiation and progression of human cancer. However, information about ovarian cancer-related miRNA is mostly limited to tissue miRNA. The aim of this study was to find specific profiles of plasma-derived miRNAs of ovarian cancer. In this present study, the expression profiles of 740 miRNAs in plasma from 18 patients and 24 healthy women subjects were evaluated using microfluidic based multiplex qRT-PCR. Our results demonstrated that expression levels of eight miRNAs were significantly upregulated in patients with ovarian cancer when compared with a control group (p < 0.05). Expression levels of four miRNAs were found significantly downregulated in patients with ovarian cancer (p < 0.05). In addition, 10 miRNAs were expressed only in the ovarian cancer group and miR-138-5p of these miRNAs is ovarian specific. In conclusion, our study suggests that detecting these ovarian cancer specific miRNAs in plasma might serve as novel non-invasive biomarkers for ovarian cancer.

N-acetylcysteine ameliorates nitrosative stress on radiation-inducible damage in rat liver.

PURPOSE: The present study was designed to investigate the potential radioprotective effects of N-acetylcysteine (NAC) on radiation-induced nitrosative stress caused by gamma irradiation (single dose, 6 Gy) in rat liver. METHODS: The rats (n=40) were divided randomly and equally into 4 groups: Control (C), Radiation (R), R+NAC (received irradiation and 1,000 mg/kg of NAC) and R+WR-2721 (received irradiation and 200 mg/kg of WR-2721). Liver tissue of each animal was harvested and utilized for 3-nitrotyrosine (3-NT) detection using high-performance liquid chromatography- ultraviolet (HPLC-UV) system. RESULTS: In the R rats, 3-NT levels significantly increased when compared to those of the C rats (p<0.05). There were no significant differences in the 3-NT levels among R+NAC and R+WR-2721 rats. Histologically examined liver tissue samples showed no obvious differences. CONCLUSION: The present study suggests that irradiation has a negative effect on the cellular proteins by enhancing 3-NT formation. The prophylactic use of NAC seems to reduce the nitrosative damage during radiotherapy.

Role of CYP2C9 and CYP2C19 polymorphisms in patients with atherosclerosis.

The arachidonic acid metabolizing CYP enzymes with prominent roles in vascular regulation are epoxygenases of the two gene family which generate epoxyeicosatrienoic acids. Carriers of CYP2C9 mutant alleles exhibit a diminished CYP2C9 metabolic capacity leading to decreased endothelium-derived hyperpolarizing factors (EDHF) synthesis and an increased risk for atherosclerosis. We investigated whether the polymorphisms of CYP2C9/19 are related with atherosclerosis. We examined 108 patients having angioraphically > or =70 coronary artery narrowing and 90 healthy controls. CYPC2C9/19*2 and CYP2C9/19*3 alleles were investigated in both patients and controls by a real time PCR instrument. There was no significant difference in the distribution of the CYP2C9*2/*3 alleles between cases and the controls. We found that smoker patients having CYP2C9*2 heterozygote genotype have 3.7-fold risk of developing atherosclerosis. CYP2C19*3 heterozygote alleles are more frequent in patients than in controls (10.2%, 5.6% respectively) and it is related with a three-fold risk of atherosclerosis (odds ratio (OR) = 3.75, confidence interval (CI) = 0.75-18.65). It becomes clear that cigarette smoking can cause almost all major diseases prevalent today, such as cancer or heart disease. This inter-subject variability in cigarette-induced pathologies is partly mediated by genetic variants of genes that may participate in detoxification processes, e.g., cytochrome P450 (CYP), cellular susceptibility to toxins, such as p53, or disease development such as atherosclerosis.

Effects of levosimendan on myocardial ischaemia-reperfusion injury.

BACKGROUND AND OBJECTIVE: Levosimendan has a cardioprotective action by inducing coronary vasodilatation and preconditioning by opening KATP channels. The aim of this study was to determine whether levosimendan enhances myocardial damage during hypothermic ischaemia and reperfusion in isolated rat hearts. METHODS: Twenty-one male Wistar rats were divided into three groups. After surgical preparation, coronary circulation was started by retrograde aortic perfusion using Krebs-Henseleit buffer solution and lasted 15 min. After perfusion Group 1 (control; n = 7) received no further treatment. In Group 2 (non-treated; n = 7), hearts were arrested with cold cardioplegic solution after perfusion and subjected to 60 min of hypothermic global ischaemia followed by 30 min reperfusion. In Group 3 (levosimendan treated; n = 7), levosimendan was added to the buffer solution during perfusion and the hearts were arrested with cold cardioplegic solution and subjected to 60 min of hypothermic global ischaemia followed by 30 min reperfusion. At the end of the reperfusion period, the hearts were prepared for biochemical assays and for histological analysis. RESULTS: Tissue malondialdehyde levels were significantly lower in the levosimendan-treated group than in the non-treated group (P = 0.019). The tissue Na+-K+ ATPase activity was significantly decreased in the non-treated group than in the levosimendan-treated group (P = 0.027). Tissue myeloperoxidase (MPO) enzyme activity was significantly higher in the non-treated group than in the levosimendan-treated group (P = 0.004). Electron microscopic examination of the hearts showed cardiomyocytic degeneration at the myofibril, mitochondria and sarcoplasmic reticulum in both non-treated and levosimendan-treated groups. The severity of these findings was more extensive in the non-treated group. CONCLUSIONS: Treatment with levosimendan provided better cardioprotection with cold cardioplegic arrest followed by global hypothermic ischaemia in isolated rat hearts.

Evaluation of the plasma microRNA levels in stage 3 premature retinopathy with plus disease: preliminary study.

PurposeIn the present study, we aimed to investigate the changes in plasma microRNA (miRNA) levels in premature infants diagnosed with premature retinopathy (ROP).Patients and methodsIn order to investigate the relationship of miRNAs with ROP, 13 premature infants admitted to Mersin University, Medical School, Department of Ophthalmology and diagnosed with ROP stage 3 with plus disease between January 2014-January 2015 were included in the study. Control group consisted of 15 premature infants with no ROP. The plasma miRNA levels were evaluated using high-throughput quantitative real-time PCR.ResultsThe results of study demonstrated that the expression level of miR-23a and miR-200b-3p was significantly upregulated in patients with ROP when compared with the control group (P<0.05). The expression level of miR-27b-3p and miR-214-3p was significantly downregulated in patients (P<0.05). In addition, expression of 17 miRNA (miR-410-3p, miR-17-5p, miR-451a, miR-31-5p, miR-132-3p, miR-183-5p, miR-184, miR-222-3p, miR-296-5p, miR-200a-3p, miR-328-3p,miR-96-5p, miR-199a-5p, miR-99a-5p, miR-106a-5p, miR-125b-5p, miR-155-5p) had upregulated or downregulated, but not statistically significantly different when compared with the control group.ConclusionsOur results suggest that plasma miRNA levels may alter in ROP and, some miRNAs might have an effect in the physiopathology of this disease. These molecules may have an important therapeutic role in patients who are unresponsive to anti-vascular endothelial growth factor therapy. However, further studies must be conducted for possible effects of miRNAs in vascular disorders of eye such as ROP. Moreover to define the relationship of these molecules with the disease more clearly, a multicenter study including more patients is necessary.

CYP2C19 polymorphisms in patients with gastric and colorectal carcinoma.

BACKGROUND: It has been reported that up to 80% of human cancers arise as a consequence of environmental exposure and host susceptibility factors. Environmental carcinogens are predominantly metabolized by the cytochrome P450 (CYP) superfamily of drug- or xenobiotic-metabolizing enzymes. Genetic variations in these enzymes affect individuals' susceptibility to carcinogens. AIM OF THE STUDY: The aim of this study was to evaluate the relationship between CYP2C19 polymorphism and susceptibility to these cancers by means of CYP2C19 genotyping among Turkish subjects. METHODS: DNAof subjects were isolated from leukocytes by high pure template preparation kit (Roche Diagnostics, GmbH, Mannheim, Germany) and genotypes were detected by LightCycler CYP2C19 Mutation Detection Kit by real-time PCR with LightCycler instrument (Roche Diagnostics, cat. no. 3113914). RESULTS: Being male was associated with a 3.5-fold (OR: 4.27, CI: 2.27-8.05) and 4.27-fold (OR: 3.50, CI: 1.948-6.301) risk for colorectal and gastric carcinoma, respectively. The CYP2C19*3 heterozygote genotype was not found in either gastric or colorectal carcinoma patients. Although the frequency of CYP2C19*2 heterozygote genotype is high in patients with gastric and colorectal carcinoma, it is not significantly associated with cancer (OR: 1.79, CI: 0.829-3.865 and OR: 1.998, CI: 0.961-4.154, respectively). CONCLUSION: Although the frequency of CYP2C19*2 heterozygote genotype is high in our patients with gastric and colorectal carcinoma, there is no the relationship between CYP2C19 polymorphism and susceptibility to these cancer.

Glutathione S-transferase M1, T1, and P1 gene polymorphism in exudative age-related macular degeneration: a preliminary report.

PURPOSE: To elucidate whether the gene polymorphisms of glutathione S-transferase (GST) M1, T1, and P1 are associated with the development of exudative age-related macular degeneration. METHODS: The authors genotyped 35 white patients with exudative age-related macular degeneration and 159 healthy controls. Genomic DNA from peripheral blood was examined using polymerase chain reaction and defined for the genetic polymorphisms of GST. RESULTS: No association was observed between GSTM1, GSTT1, and GSTP1 polymorphisms and age-related macular degeneration risk (p>0.05). The frequencies of the combination of the GSTM1 (null) and GSTP1 (mutant), GSTM1 (null), and GSTT1 (null) genotype polymorphisms in patients with exudative age-related macular degeneration differed greatly from those of the control group (p=0.001 OR [95% CI]: 7.70 [2.28-25.98] and p=0.007 OR [95% CI]: 3.88 [1.51-10.02], respectively). CONCLUSIONS: The present study suggests that the GSTM1 (null) and GSTT1 (null), GSTM1 (null), and GSTP1 (mutant) combinations may be a genetic risk factor for the development of exudative age-related macular degeneration. However, the potential role of GST polymorphisms as a marker of susceptibility to age-related macular degeneration needs further studies in a larger number of patients.

Serum L-carnitine levels and lipoprotein compositions in chronic viral hepatitis patients.

OBJECTIVES: The aim of this study was to evaluate the serum L-carnitine levels and its effect on lipoproteins in chronic viral hepatitis B or C patients. DESIGN AND METHODS: Blood samples were taken from 41 patients and 30 healthy subjects after 12 h fasting. RESULTS: Patients' serum L-carnitine levels (11.19 +/- 6.67 mg/L) (p < 0.0001) and hepatic enzyme activities (AST and ALT) (49.02 +/- 42.80 and 58.35 +/- 57.51 U/L) (p < 0.0005) were significantly higher than controls'. Serum total (3.85 +/- 0.82 mmol/L), LDL (2.08 +/- 0.76 mmol/L) and HDL (1.02 +/- 0.29 mmol/L) cholesterol levels were significantly lower in patients (p < 0.01). On the other hand triglyceride levels (1.65 +/- 0.85 mmol/L) were significantly higher in patients (p < 0.05). CONCLUSIONS: The higher L-carnitine levels of patients may result from the leakage of hepatic cellular carnitine. If there is a decreased hepatic cellular carnitine levels, this may affect the transport of acetyl moiety for cholesterol synthesis and alter lipoprotein composition. Further investigation is needed for hepatic tissue L-carnitine levels.

Effect of anti-rat interleukin-6 antibody after spinal cord injury in the rat: inducible nitric oxide synthase expression, sodium- and potassium-activated, magnesium-dependent adenosine-5'-triphosphatase and superoxide dismutase activation, and ultrastructural changes.

OBJECT: The inflammatory cells that accumulate at the damaged site after spinal cord injury (SCI) may secrete interleukin-6 (IL-6), a mediator known to induce the expression of inducible nitric oxide synthase (iNOS). Any increased production of NO by iNOS activity would aggravate the primary neurological damage in SCI. If this mechanism does occur, the direct or indirect effects of IL-6 antagonists on iNOS activity should modulate this secondary injury. In this study, the authors produced spinal cord damage in rats and applied anti-rat IL-6 antibody to neutralize IL-6 bioactivity and to reduce iNOS. They determined the spinal cord tissue activities of Na+-K+/Mg++ adenosine-5'-triphosphatase (ATPase) and superoxide dismutase, evaluated iNOS immunoreactivity, and examined ultrastructural findings to assess the results of this treatment. METHODS: Seventy rats were randomly allocated to four groups. Group I (10 rats) were killed to provide normal spinal cord tissue for testing. In Group II 20 rats underwent six-level laminectomy for the effects of total laminectomy alone to be determined. In Group III 20 rats underwent six-level T2-7 laminectomy and SCI was produced by extradural compression of the exposed cord. The same procedures were performed in the 20 Group IV rats, but these rats also received one (2 microg) intraperitoneal injection of anti-rat IL-6 antibody immediately after the injury and a second dose 24 hours posttrauma. Half of the rats from each of Groups II through IV were killed at 2 hours and the other half at 48 hours posttrauma. The exposed cord segments were immediately removed and processed for analysis. CONCLUSIONS: The results showed that neutralizing IL-6 bioactivity with anti-rat IL-6 antibody significantly attenuates iNOS activity and reduces secondary structural changes in damaged rat spinal cord tissue.

The effect of collagen, interleukin-1 alpha and glicosaminoglycan on the neovascularization of central nervous system.

Neovascularization, the development of a new microvasculature, has an important role in physiological and pathological processes. The vascular changes in the brain can be easily detected because the proliferation of endothelial cells in its vascular structure is quite small, and so constitutes a good model for neovascularization studies. In the present investigation, to induce intracerebral neovascularization, we implanted collagen, Interleukin-1 alpha (IL-1 alpha) and glicosaminoglycan into the brain of pigs, in order to test the hypothesis that IL-1 alpha, collagen and glicosaminoglycan play a pivotal role in the process of neovascularization. Both pure collagen and collagen combined with IL-1 alpha induced neovascularization according to light-electron microscopic findings and values of enzymes' activities. In particular, collagen combined with IL-1 alpha synergically affected the increase of neovascularization. However, glicosaminoglycan did not affect it significantly. Although the results of this study provided us with some interesting data indicating the beneficial effects of collagen combined with IL-1 alpha on neovascularization, further studies should be done to study the short term effect of these biochemical substances.

Serum copper, zinc and magnesium levels in children with enterobiosis.

Levels of serum copper (Cu), zinc (Zn) and magnesium (Mg) were determined in the sera of 250 children aged between 6 and 13. Of these children, 180 were infected only with Enterobius vermicularis. The remaining 70 children were without parasitic or bacterial infection and made up the control group. The cellophane tape method was used to detect E.vermicularis infection. The levels of Cu, Zn and Mg in the serum samples were measured with the Perkin- Elmer 2380 Atomic Absorption Spectrophotometer. Evaluation by the student-t test showed that the means of the Cu, Zn and Mg in the serum were significantly lower in the infected group than in the control group. Thus, in this study, we found that E. vermicularis adversely affects the level of elements such as Cu, Zn, and Mg in serum.

The relationship between leptin and lipids in atherosclerosis.

BACKGROUND: This study aimed to examine the extent to which leptin, alone or in combination with other risk factors, may be an independent marker for myocardial infarction in a region with a high incidence of cardiovascular disease. METHODS AND RESULTS: Leptin levels were measured by the ELISA method, while plasma lipids and lipoproteins were measured by conventional methods. Leptin levels were significantly higher in the patient than in the control group. Serum total cholesterol, low-density lipoprotein, lipoprotein (a) and apolipoprotein B showed a significant correlation with leptin, while high-density lipoprotein showed an inverse relation. CONCLUSIONS: Our results suggest that leptin may be one factor operating in the metabolic alteration taking place during myocardial infarction, and is a possible risk factor.

Levels of malondialdehyde, glutathione and ascorbic acid in idiopathic thrombocytopaenic purpura.

BACKGROUND: Idiopathic thrombocytopaenic purpura (ITP) is an autoimmune disorder, which causes an acute or chronic thrombocytopenia, and may result in potentially life-threatening haemorrhage. Oxidative damage may be involved in the pathogenesis of autoimmune diseases. Antibodies to bind to membrane lipids and platelet destruction may play a role on lipid peroxidation in ITP. OBJECTIVES: To investigate the posible role of lipid peroxidation and antioxidants in patients with ITP. DESIGN: The levels of plasma and erythrocyte malondialdehyde (MDA), erythrocyte glutathione and ascorbic acid were analysed in patients with ITP. METHODS. The MDA levels were performed according to the method of Bidlack WR. Plasma MDA, erythrocyte glutathione and ascorbic acid levels were carried out according to the methods of Ohkawa H, Beutler E and Bauer JD, respectively. RESULTS: The erythrocyte and plasma MDA levels in patients with ITP were found to be 9.52+/-4.65, 3.03+/-1.44 (p<0.001) and in control group were found to be 2.49+/-0.57, 1.03+/-0.28 nmol/ml (p<0.001), respectively. Erythrocyte glutathione was found to be 3.71+/-0.82, 6.26+/-0.66 micromol/gr Hb (p<0.001). Ascorbic acid levels of these groups were 1.09+/-0.25, 1.70+/-0.33 mg/dl (p<0.001). CONCLUSION: The oxidative damage is involved in the pathogenesis of ITP. In patients with ITP, the platelet destruction and bleeding may play significant role on elevation of lipid peroxidation and reduction of antioxidant capacity. Further studies on oxidant and antioxidant status of ITP are also needed to confirm these results.

Trace elements and vitamin levels in menopausal women receiving hormone replacement therapy.

Trace elements are extremely important in human metabolism, growth, and tissue repair. The risk of nutritional disturbances, in particular, vitamin and trace element deficiencies, are striking during menopause. The aim of this longitudinal study was to evaluate the effect of estrogen treatment on serum levels of copper, zinc, magnesium, calcium, vitamin E, and vitamin A in menopausal women. Thirty-eight menopausal women were included in the study, and were administered a continuous hormone replacement therapy (HRT) of 0.625 mg conjugated equine estrogen (CEE) and 2.5 mg medroxyprogesterone acetate (MPA). Blood samples were obtained before and six months after HRT. There was a statistically significant difference between levels of serum copper, zinc, magnesium, calcium, vitamin E and vitamin A before and after HRT (p < 0.001). In conclusion we observed a beneficial effect of HRT on serum levels of trace elements, vitamin A, and vitamin E in addition to the well known other benefits.

Apolipoprotein B gene polymorphisms in people in the east Mediterranean area of Turkey.

Point mutations in the receptor binding domain of low density lipoprotein may increase cholesterol levels in blood. Three mutations of Apo B-100 protein result in defective binding (Arg 3500 ----> [corrected] Gln, Arg 3500 ----> [corrected] Trp and Arg 3531 ----> [corrected] Cys). We estimated the frequency of Apo B point mutations (codon 3500) C9774T (Arg 3500 ----> [corrected] Trp) and G9775A (Arg 3500 ----> [corrected] Gln) in 179 atherosclerotic, 145 hyperlipidaemic individuals and 272 healthy individuals in the east Mediterranean region of Turkey. Lipid and lipoprotein levels were measured with routine biochemical analyser and Apo B mutation was detected using real-time PCR. Neither mutation was found. In this region, Apo B-100 protein mutations are rare and causes of hyperlipidaemia and atherosclerosis may therefore be unrelated to them.

The Levels of Sera Malondialdehyde, Erythrocyte Membrane Na+-K+/Mg++ and Ca++/Mg++ Adenosine 5' Triphosphatase in Patients with Sickle Cell Anemia.

The various membrane abnormalities of sickle erythrocytes may result from excessive accumulation of oxidant damage. We measured the sera levels of malondialdehyde, products of lipid peroxidation, Na+-K+/Mg++ Adenosine 5' triphosphatase (ATPase) and Ca++/Mg++ Adenosine 5' triphosphatase, erythrocyte membrane enzymes, in patients with sickle cell anemia and compared their levels with that of normal controls. MDA, Na+-K+/Mg++ and Ca++/Mg++ ATPase levels of control groups were 0.90 ± 0.04 nmol/mL, 168 ± 12.9 and 140.6 ± 8.2 nmol Pi/mg prot/hour, respectively. MDA, Na+-K+/Mg++ and Ca++/Mg++ATPase levels of patients were 2.02 ± 0.01 nmol/mL, 127.0 ± 8.4 and 110.0 ± 9.6 nmol Pi/mg prot/hour, respectively. Our experimental results showed that there was a significant increase in MDA levels of patients with sickle cell anemia as compared with that of the controls. However, erythrocyte membrane Na+-K+/Mg++ and Ca++/Mg++ ATPase levels of patients with sickle cell anemia were significantly lower than the, Na+-K+/Mg++ and Ca++/Mg++ ATPase levels of normal controls.

Inhibition of extracellular signal-regulated kinase (ERK1/2) activity reverses endotoxin-induced hypotension via decreased nitric oxide production in rats.

Overproduction of reactive oxygen and nitrogen species leads to oxidative stress and decreased total antioxidant capacity, which is responsible for high mortality from several inflammatory diseases such as endotoxic shock. Among reactive nitrogen species, nitric oxide (NO) produced by inducible NO synthase (iNOS) during endotoxemia is the major cause of vascular hyporeactivity, hypotension and multiple organ failure. This study was conducted to determine if mitogen-activated protein kinases (MAPKs) such as extracellular signal-regulated kinase (ERK1/2) contributes to endotoxin-induced hypotension as well as vascular inflammation and oxidative stress via NO production. In conscious male Wistar rats, injection of endotoxin (10 mg kg(-1), i.p.) caused a decrease in mean arterial pressure (MAP) for 4h and increased levels of nitrite in serum, aorta and mesenteric artery. These effects of endotoxin were prevented by selective inhibition of ERK1/2 phosphorylation by MAPK kinase (MEK1/2) with U0126 (5 mg kg(-1), i.p.; 1h after endotoxin). Endotoxin also caused an increase in protein levels of phosphorylated ERK1/2 in aorta which was abolished by U0126. Selective inhibition of iNOS with phenylene-1,3-bis[ethane-2-isothiourea] dihydrobromide (1,3-PBIT) (10 mg kg(-1), i.p.; 1h after endotoxin) did not change the endotoxin-induced increase in ERK1/2 activity. Myeloperoxidase activity was increased in aorta and decreased in mesenteric artery by endotoxin, which was reversed by U0126. Endotoxin-induced decrease in one of the products of lipid peroxidation, malonedialdehyde (MDA) was prevented by U0126 in mesenteric artery; however, U0126 caused a further decrease in the levels of MDA in aorta. These data suggest that increased phosphorylation of ERK1/2 by MEK1/2 contributes to the endotoxin-induced hypotension via NO production rat aorta and mesenteric artery. It is likely that ERK1/2 mediates the effect of endotoxin on MPO activity in a different degree in the tissues suggesting possible involvement of any mediator and/or mechanism which also causes neutrophil infiltration during inflammatory response at least in mesenteric artery. Moreover, ERK1/2 seems to be involved in the endotoxin-induced increase in total antioxidant capacity in mesenteric artery.

Effects of Nigella orientalis and N. segetalis fixed oils on blood biochemistry in rats.

Nigella orientalis and N. segetalis fixed oils were administered orally (1 mL/kg/day) to Wistar Kyoto rats for 4 weeks. The effects of the oils on biochemical parameters were compared with a control group that received distilled water under identical conditions. LDL-cholesterol level was decreased significantly in both oil groups while serum total cholesterol and VLDL-cholesterol were decreased significantly following administration of only N. orientalis fixed oil when compared with the control group. The HDL-cholesterol levels were increased significantly in both oil groups.N. orientalis fixed oil significantly reduced Aspartateaminotransferase (AST), Alkaline Phosphatase (ALP), bilirubin and urea levels in rats. There was an increase in the albumin, uric acid and mean corpuscular volume (MCV) concentrations, while the mean corpuscular hemoglobin concentration (MCHC) and RDW (red cell distribution width) levels decreased significantly. In N. segetalis fixed oil treated rats, the levels of ALP, Blood Urea Nitrogen (BUN), MCHC, RDW were decreased significantly, whereas a significant increase was found in albumin, fibrinogen, Hematocrit (HCT) and MCV levels. The effects of 4 weeks oral intake of N. orientalis and N. segetalis fixed oils on blood malondialdehyde (MDA) and total antioxidant status (TOS) were also investigated in rats. The study showed that the oils had no significant effect on MDA production. N. orientalis and N. segetalis fixed oils caused a significant increase in the total antioxidant status in rats.