N-acetylcysteine prevents doxorubucine-induced cardiotoxicity in rats.

This study is designed to observe the effects of N-acetylcysteine (NAC) on doxorubucine-induced cardiac toxicity in rats both histologically and biochemically. Totally 32 rats divided equally into four groups were studied. The first group received only 200 mg/kg NAC intraperitoneal (i.p.) once every 24 h for 5 days (group 1); the second group received 20 mg/kg doxorubucine (DOX) i.p. single dose plus NAC 200 mg/kg i.p. once every 24 h for 5 days (group 2); the third group received DOX 20 mg/kg DOX i.p. single dose (group 3) and the fourth group, which is also the control group, received saline (group 4). Following 24 h of the final dose, blood samples were drawn from a portal vein and heart tissue were obtained. Tissue thiobarbituric acid reactive substance (TBARS) and nitric oxide (NO) levels were highest in the DOX group. In the DOX-treated rats, serum TBARS, NO, aspartate transaminase, lactate dehydrogenase and creatine kinase levels were highest when compared with other groups. Except for serum superoxide dismutase levels, all other parameters differed significantly between the DOX plus NAC group and the DOX group. In the DOX plus NAC group, general architecture was preserved better than the DOX group and myofibril loss was minimal compared with the DOX group. NAC demonstrated, both biochemically and histologically, to be effective in the prevention of DOX-induced cardiotoxicity in rat models. Evaluation of NAC's effect on DOX toxicity warrants further clinical trials on cancer patients.

The scintigraphic evaluation and genetic correlation of joint involvements in pediatric patients with familial Mediterranean fever.

PURPOSE: We aimed to evaluate the articular involvements in pediatric patients with familial Mediterranean fever (FMF) with joint symptoms by bone scintigraphy and to correlate the involved joints with the gene mutations. MATERIALS AND METHODS: A total of 41 newly diagnosed patients in pediatric age group (28 girls and 13 boys; mean age 9.14 ± 2.91 years) with joint involvement symptoms were included in this study. Scintigraphic images were obtained at 5th min (blood pool or early phase) and starting at 3 h (late phase) after (after tracer injection) intravenous administration of technetium-99m (99mTc)-methylendiphosphonate (MDP). Genomic DNA was isolated from leukocytes using standard salting out procedure. The sequencing data were analyzed. RESULTS: Of the 41 patients, arthritis was found in 21 (51.2%) patients. Of the 21 patients, there was single joint involvement in 15 (71.4%) patients and multiple joint involvement in six (28.6%) patients. The mean age of patients with joint involvement (8 ± 2.3 years) were considerably lower than the patients without joint involvement (10.35 ± 3.04 years), and this was statistically significant (p = 0.008). The most commonly involved joints were ankles and knees. Multiple joint involvements were most frequently observed in the M694V and M694I gene mutations (16.7%). CONCLUSIONS: We use and recommend the bone scintigraphy in patients with FMF to determine the presence and distribution of arthritis, since bone scintigraphy is inexpensive, noninvasive, easy-to-use, and also is more sensitive in the diagnosis and distribution of arthritis than conventional radiological methods and clinical examination.

Protective effects of thymoquinone on vancomycin-induced nephrotoxicity in rats.

AIM: Oxidative stress has been implicated as a potential responsible mechanism in the pathogenesis of vancomycin (VCM)-induced renal toxicity. Therefore, we aimed to investigate the protective effect of thymoquinone (TQ) against VCM-induced nephrotoxicity by tissue oxidant/antioxidant parameters and histological changes in rats. MATERIALS AND METHODS: Wistar albino rats were randomly separated into four groups consisting of seven rats per group. The groups had normal saline (control group), VCM, VCM and TQ and TQ, respectively. VCM was injected intraperitoneally at a dose of 200 mg/kg and continued at 12-h intervals for 7 days. TQ was injected intraperitoneally at a dose of 10 mg/kg and continued at 24 h intervals for 8 days. Animals were killed and blood samples were analyzed for the levels of serum blood urea nitrogen (BUN) and creatinine (Cr). Kidney specimens were analyzed for levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as for histopathological changes. RESULTS: We found that the levels of serum BUN, Cr and kidney tissue MDA were increased in the VCM group. Activities of SOD and GSH-Px in kidney tissue were decreased. TQ administration ameliorated significantly these changes. CONCLUSION: These results indicate that the TQ produces a protective mechanism against VCM-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

Effects of erdosteine on cyclosporin-A-induced nephrotoxicity.

AIM: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. MATERIALS AND METHODS: Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. RESULTS: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. CONCLUSION: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

Brucellosis with very high ferritin levels: report of five cases.

Brucellosis is a zoonotic disease caused by a kind of Brucella bacteria, which commonly appears in humans and rarely causes mortality. In our study, five cases, who were diagnosed by evaluation of clinical findings and serological tests, they also had very high ferritin levels, were reported. Ages of the patients were 16, 12, 10, 16 and 8 years, respectively. Serum ferritin levels were 1200, 985, 886, 748 and 435 ng/ml, respectively. We observed that complaints of the patients reduced after the treatment and ferritin levels returned to its normal range. In the situations of extremely evaluated serum ferritin which is an acute-phase reactant, its levels are able to raise in brucellosis, without existing hemochromatosis and Still's disease.

Effects of erdosteine on hemostasis: an experimental study.

AIM: In this study, the effects of erdosteine (ED) on the platelet function and coagulation were investigated in adult rats. MATERIALS AND METHOD: Twenty-eight male Wistar albino rats were divided into four groups. The control rats in group I (n = 7) were given only 0.5 cc of normal saline daily through oral gavage. Group II (n = 7) rats were administered 3 mg/kg ED through oral gavage for 3 days; while group III (n = 7) rats were given 10 mg/kg ED through oral gavage for 3 days; and group IV (n = 7) rats were administered 30 mg/kg ED through oral gavage for 3 days. Prothrombin time (PT), activated prothromboplastin time (aPTT), international normalized ratio (INR), coagulation factors and complete blood counts were measured from the blood drawn. RESULTS: There were a lot of differences between ED groups and control group, and among ED groups. The found differences were level of PT, aPTT, INR, coagulation factors, and number of platelets. DISCUSSION: We consider that ED which is used as a mucolytic agent in child clinics may affect hemostasis and coagulation in a dose-dependent manner. ED should be used carefully by the patients with coagulation disorders, since there is no information available in the package insert and literature screening regarding the effect of ED.

Ala-9Val polymorphism of Mn-SOD gene in sickle cell anemia.

Oxidative stress may be contributory to the pathophysiology of the abnormalities that underlie the clinical course of sickle cell anemia. We looked for a possible genetic association between the functional polymorphism Ala-9Val in the human Mn-SOD gene and sickle cell anemia. One hundred and twenty-seven patients with sickle cell anemia and 127 healthy controls were recruited into the study. Alanine versus valine polymorphism in the signal peptide of the Mn-SOD gene was evaluated using a primer pair to amplify a 107-bp fragment followed by digestion with the restriction enzyme NgoMIV. In the sickle cell anemia patients, the frequency of Val/Val genotype was approximately 1.4-fold lower and that of Ala/Val was 1.3-fold higher compared to the controls. No significant difference in genotype frequencies was found between patients and controls (χ(2) = 4.561, d.f. = 2, P = 0.101). The Val-9 was the most common allele in patient and healthy subjects. No significant difference in allele frequencies was found between patients and controls (χ(2) = 1.496, d.f. = 1, P = 0.221). We conclude that the Mn-SOD gene polymorphism is not associated with sickle cell anemia.

Pediatric poisonings in southeast of Turkey: epidemiological and clinical aspects.

Current detailed information about the causes, management, and clinical course of acute childhood poisonings in Turkey is scarce. Therefore, we have conducted a descriptive study of children presenting with acute poisoning to the pediatric emergency department of Dicle University Hospital throughout an 8-month period. Two hundred unselected children with poisoning were evaluated in terms of clinical, epidemiological and socioeconomic aspects. The mean age of patients was 5.7 +/- 4.0 years. The majority of the patients (n = 108, 54%) were aged from 13 months to 4 years (P < 0.05). In majority of patients (66.5%, n = 133), poisonings were accidental. Intentional poisonings accounted for 3.5% (n = 7) and food poisoning accounted for 30% (n = 60) of all cases. The families had more than three children in 129 (97%) of accidentally poisoned and in seven (100%) of intentionally poisoned patients, six were girls and one was a boy. The parents of most patients were uneducated. Furthermore, more than two third of families had low level of income. In all, 171 patients (85.5%) were discharged after an observation period of 24 h. Four patients died. In conclusion, factors such as low educational level of parents, presence of more than three children in the family, and low income increase the incidence of childhood poisonings. The low educational level of girls increases the incidence of intentional poisoning.