Suleyman Oktar

High plasma nesfatin-1 level in patients with major depressive disorder

AIM In the present study, our aim was to determine the changes in the plasma concentrations of a recently discovered peptide hormone nesfatin-1 in patients with major depressive disorder and then to make a comparison with the control group. METHOD Subjects in the patient group were randomly selected from Mustafa Kemal University, Medical School, Research and Training Hospital, Psychiatry Department, Outpatient Clinic and subjects in the control group were selected from healthy volunteers. Healthy control subjects were matched in terms of weight and body mass index. Hamilton Depression Rating Scale (HAM-D) was applied to both groups. ELISA method was used for measurement of plasma nesfatin-1 levels. RESULTS The average nesfatin-1 level was statistically higher in patients with major depressive disorder than in the control group (p<0.001). A positive correlation was observed between plasma nesfatin-1 levels and HAM-D scores both in the patient group (r=0.59, p<0.001) and in the control group (r=0.58, p<0.001). CONCLUSION Our findings suggest a possible relationship between major depressive disorder and high plasma nesfatin-1 level.

Protective effects of tadalafil on experimental spinal cord injury in rats

Tadalafil is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5). Nitric oxide (NO) functions as a retrograde neurotransmitter in the spinal cord, and postsynaptic structures respond to NO by producing cGMP. The concentrations of cGMP in the spinal cord are controlled by the actions of PDE. The aim of the study was to evaluate and compare the effects of the use of both methylprednisolone and tadalafil on serum and tissue concentrations of NO, malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, and tissue glutathione peroxidase (GSH-Px) activity in rats with spinal cord injury (SCI). SCI was induced in Wistar albino rats by dropping a 10 g rod from a 5.0 cm height at T8-10. The 28 rats were randomly divided into four equal groups: tadalafil, methylprednisolone, non-treatment and sham groups. Rats were neurologically tested at 24 hours after trauma. At the end of the experiment, blood samples were collected and spinal cord tissue samples were harvested for biochemical evaluation. The tissue level of NO was increased in the tadalafil group compared with the non-treatment and methylprednisolone groups (p<0.05). The tissue levels of SOD and GSH-Px did not differ between the groups. Serum levels of NO were higher in the tadalafil group than in the non-treatment group (p<0.05). The increase in serum SOD levels was greater in the tadalafil group than the methylprednisolone group. Serum MDA levels in the tadalafil and methylprednisolone groups tended to be lower than in the non-treatment group (p>0.05). Tissue MDA levels in the tadalafil and methylprednisolone groups tended to be lower than in the non-treatment group and sham groups (p>0.05). Although there was no difference in neurological outcome scores between the tadalafil, methylprednisolone and non-treatment groups (p>0.05), the animals in the tadalafil and methylprednisolone groups tended to have better scores than the non-treatment group. Thus, tadalafil appears to be beneficial in reducing the effects of injury to the spinal cord by increasing tissue levels of NO and serum activity of SOD.

Protective effects of thymoquinone against methotrexate-induced testicular injury

Thymoquinone is the major active component derived from Nigella sativa. Methotrexate is a folic acid antagonist widely used in clinic. Aim of this study was to investigate the possible protective role of thymoquinone on testicular toxicity of methotrexate. Experiments were performed on male C57BL/6 mice (6 weeks old, 20 ± 2 g). The animals were divided into four groups with six mice in each group. Equivalent volumes of saline were injected intraperitoneally (i.p.) in the control group. In the thymoquinone group, mice received thymoquinone i.p. with a dose of 10 mg/kg/day for 4 days. Mice in the methotrexate group received single dose of methotrexate i.p., with a dose of 20 mg/kg. Finally, in the methotrexate plus thymoquinone group, in the first and the following 3 days after methotrexate administration, thymoquinone was injected with a dose of 10 mg/kg/day, i.p. At the end of the experiment, the left testis was quickly removed and divided into two parts for histological examination and biochemical analysis. Methotrexate alone increased total antioxidant capacity and myeloperoxidase activity compared to the controls. Thymoquinone treatment decreased total antioxidant capacity and prevented the increase in the myeloperoxidase activity. Light microscopy showed in mice that receiving methotrexate resulted in interstitial space dilatation, edema, severe disruption of the seminiferous epithelium and reduced diameter of the seminiferous tubules. Administration of thymoquinone reversed histological changes of methotrexate significantly. We suggest that thymoquinone use may decrease the destructive effects of methotrexate on testicular tissue of patients using this agent.

The Beneficial Effects of Tadalafil on Renal Ischemia-Reperfusion Injury in Rats

Acute renal failure due to ischemia-reperfusion (I/R) injury is a common complication in cardiovascular surgery. We determined the influence of tadalafil on renal injury in a renal I/R model in rats. For this purpose, 21 male Wistar albino rats were separated into 3 groups: sham, placebo and tadalafil. A right nephrectomy was performed, and the left renal pedicles were occluded for 60 min and reperfused for 60 min in the placebo and tadalafil groups. A single dose of tadalafil (10 mg/kg) through an orogastric tube was administered to the tadalafil group. Tubular atrophy with acute inflammation in renal histology, total oxidant status (TOS) and total antioxidant status (TAS) were determined in tissue homogenates. Compared to the tadalafil group, tubular atrophy and acute inflammation was significant in the placebo group. TAS levels were significantly higher in the tadalafil group compared to the placebo (p = 0.01) and sham groups (p = 0.04). While TOS levels were significantly higher in the placebo group (p = 0.03), tadalafil did not significantly alter the TOS levels. The beneficial effects of tadalafil can be attributed to its protective effects on renal tubular cells and inhibition of leukocyte infiltration in renal tissue. We think that tadalafil treatment has an important role in reducing renal injury resulting from renal I/R.

Nitric oxide, lipid peroxidation, and antioxidant enzyme levels in epileptic children using valproic acid.

In the present study, we investigated the effects of valproic acid (VPA) on nitric oxide (NO) level, lipid peroxidation, and antioxidant enzyme activities in 21 epileptic children and 26 healthy controls. The subjects were selected from those who visited for a checkup or medical treatment at the Mustafa Kemal University Research Hospital. Serum levels of NO(-2), NO(-3), malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) were analyzed by redox or enzymatic reactions and spectrophotometry. Based on the NO(-2) and NO(-3) levels, the NO concentration was about 10% higher in VPA group than in the control group (p<0.001). However, no significant difference was detected for serum MDA, SOD, and CAT levels. It is suggested that NO would play a role in the mechanism of antiepileptic effects by VPA treatment.

Protective effect of caffeic acid phenethyl ester on cyclosporine A-induced nephrotoxicity in rats.

Introduction. Cyclosporine A, an immunosuppressive agent, is widely used after organ transplantation such as the liver and kidney. However, its widespread use is restricted because it has serious toxic effects on the kidney. Caffeic acid phenethyl ester (CAPE) is a natural product with potent anti-inflammatory, antitumor, and antioxidant activities, and it attenuates inflammation and lipid peroxidation induced by ischemia-reperfusion injury. The purpose of the present study was to investigate the effects of CAPE on cyclosporine A (CsA)-induced nephrotoxicity. Material and Methods. Rats were divided into four groups and treated with saline, CAPE, CsA, and CsA + CAPE. Control rats were given saline; the CAPE group was given CAPE (10 μmol/kg/day) for 11 days intraperitoneally; the CsA group was given CsA (15 mg/kg/day) for 10 days subcutaneously; and the CsA+CAPE group was given CAPE for 11 days, and rats were s.c. injected with CsA in 0.5 ml of saline once a day for 10 days at the same time. Results. The administration of CsA alone resulted in higher myeloperoxidase (MPO) activity, lipid peroxidation, superoxide dismutase (SOD), and catalase (CAT) than in the control. The enzyme activities except CAT in rats treated with CAPE alone were not changed. CAPE treatment prevented the increase in malondialdehyde (MDA) and increased CAT activity more, but did not affect the activities of MPO and SOD enzymes. Discussion. CsA causes renal injury and CAPE prevents CAT- and lipid peroxidation-mediated nephrotoxicity via inhibition of oxidative process.

Ceftriaxone ameliorates cyclosporine A-induced oxidative nephrotoxicity in rat.

A growing body of evidence now suggested that cyclosporine A (CycA)‐induced nephrotoxicity is a crucial clinical problem and oxidative stress is importantly responsible for its toxicity. Ceftriaxone induced antioxidant effect in brain and neuronal tissues against oxidative damage although its antioxidant potential effect on kidney has not been clarified. The aim of this study was to evaluate whether ceftriaxone protects CycA‐induced oxidative stress kidney injury in rats. Twenty‐four rats were equally divided into four groups. First group was used as control. Ceftriaxone (200 mg/kg) and CycA (15 mg/kg) were administrated to second and third groups for 10 days, respectively. The ceftriaxone and CycA combination was given to rats constituting the fourth group for 10 days. Lipid peroxidation (LP), urea nitrogen and lactate dehydrogenase (LDH) levels were higher in CycA group than in control and ceftriaxone groups although LP, urea nitrogen and LDH levels were lower in ceftriaxone + CycA group than in control and ceftriaxone groups. Glutathione peroxidase and catalase activities were lower in CycA group than in control whereas their activities were increased in control and ceftriaxone groups. Superoxide dismutase activity did not change by the treatments. Ceftriaxone administration recovered also CycA‐induced atrophy, vacuolization and exfoliations of tubular epithelium and glomerular collapse in histopathological evaluation of kidney. In conclusion, we observed that ceftriaxone is beneficial on CycA‐induced oxidative stress in kidney of rats by modulating oxidative and antioxidant system. Copyright

Direct and indirect effects of kisspeptin on liver oxidant and antioxidant systems in young male rats

Kisspeptin is a recently discovered hypothalamic peptide which plays an important role in the central control of reproductive functions. We have investigated direct and indirect effects of kisspeptin on the liver oxidative stress in young male rats. Twenty‐four rats were divided into four groups (n = 6/group). First group served as control and received saline. Kisspeptin‐10 was administered to the animals in the second group (20 nmol/rat/day), for a period of 7 days. Rats were given only one dose gosereline (0.9 mg/rat), a GnRH agonist in the third group. The last group received kisspeptin‐10 with gosereline. The activities of catalase, superoxide dismutase (SOD), xanthine oxidase (XO), adenosine deaminase (AD) and level of malondialdehyde were studied in liver tissue. Serum samples were separated for total antioxidant capacity (TAC), total oxidant status (TOS), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, blood urea nitrogen (BUN), colesterol, high‐density lipoprotein (HDL) and triglyceride. Kisspeptin increased the activities of SOD and catalase (p < 0.05). When compared to the control group, the levels of malondialdehyde, TOS and AST were lower, but levels of BUN, cholesterole, HDL and AD were higher in the other three groups (p < 0.05). In conclusion, our findings suggest that kisspeptin may have antioxidant and thus protective effects on the liver tissue. Copyright

Prazosin treatment in the management of scorpion envenomation.

Scorpion stings represent an important and serious public health problem worldwide due to their high incidence and potentially severe and often fatal clinical manifestations. Children are at greater risk of developing severe cardiac, respiratory, and neurological complications due to lesser body surface area. Alpha receptor stimulation plays important role in the pathogenesis of pulmonary edema. Prazosin, a post synaptic alpha blocker, can be recommended as an effective drug in the treatment of serious scorpion envenomations with significant sympathetic symptoms. Oral prazosin is fast acting, easily available, relatively cheap, free from any anaphylaxis and highly effective.

Effects of β-glucan pretreatment on acetylsalicylic acid-induced gastric damage: An experimental study in rats.

BACKGROUND NSAIDs have been found to induce gastrointestinal tract damage. Recently, it has been suggested that this might be mediated by lipid peroxidation. OBJECTIVE The aim of this study was to assess the potential protective effects of β-glucan against acetylsalicylic acid (ASA-induced gastric damage by means of its antioxidant capacity in an experimental rat model. METHODS Thirty-two male Wistar albino rats (200-250 g) were randomized into 4 groups consisting of 8 rats each. The β-glucan group received 50 mg/kg β-glucan once a day for 10 days and 30 minutes before anesthesia. The ASA group received saline once a day for 10 days and 300 mg/kg (20 mg/mL) ASA as a single dose, 4 hours before anesthesia. The ASA+β-glucan group was administered 50 mg/kg β-glucan once a day for 10 days and 30 minutes before anesthesia. Additionally, 300 mg/kg (20 mg/mL) ASA was administered as a single dose, 4 hours before anesthesia. The control group received saline once a day for 10 days and 30 minutes before anesthesia. All medications were administered by intragastric gavage. The stomach from each rat was dissected and divided into 2 parts for histologic and biochemical analysis. Gastric tissue malondialdehyde (MDA), nitric oxide (NO) levels, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were determined for oxidative parameter analysis. RESULTS The gastroprotective and antioxidant effects of β-glucan appeared to attenuate the ASA-induced gastric tissue damage. Compared with the control group, MDA and NO levels and CAT and GSH-Px activities were significantly increased in the stomachs of ASA-treated rats (MDA, 4.12 [0.44] to 13.41 [1.05] μmol/L; NO, 8.04 [7.25-9.10] vs 30.35 [22.34-37.95] μmol/g protein; CAT, 0.050 [0.004] to 0.083 [0.003] k/g protein; GSH-Px, 0.57 [0.42-0.66] to 1.55 [1.19-1.76] U/L; all, P < 0.001), whereas SOD activity was significantly decreased in the same group (291 [29] to 124 [6] U/mL; P < 0.001). In the ASA+β-glucan group, MDA and NO levels and CAT and GSH-Px activities were found to be significantly lower, while SOD activity was found to be significantly higher, in comparison with the ASA-treated group (all, P < 0.001). CONCLUSION β-Glucan appeared to attenuate the gastric damage caused by ASA in these rats.