Acute and subacute toxicities of biogenic tellurium nanorods in mice.

The current study was performed to evaluate the acute and subacute toxicities of biogenic tellurium nanorods (Te NRs). The Te NRs were prepared using Pseudomonas pseudoalcaligenes strain Te in a culture medium containing K2TeO3 (1 mM) and their physiochemical properties were investigated using TEM, EDX and XRD. The median lethal dose (LD50) of Te NRs and potassium tellurite (K2TeO3) were determined in mice and the subacute toxicity was also evaluated. The experimental design involved certain general toxicological, haematological, serum and histopathological investigations. The TEM and XRD analyses showed that the biogenic nanoparticles were rod-shaped and hexagonal. The toxicological evaluation showed that the LD50 values of Te NRs and K2TeO3 were 60 and 12.5 mg/kg, respectively. Higher doses of Te NRs (6 mg/kg) and K2TeO3 (1.25 mg/kg) were accompanied by signs of toxicity, including lower body weight, elevation in MDA and depletion in GSH content, SOD and CAT activity, and changes in biochemistry parameters. No obvious histopathological changes were observed in the treatment with Te NRs. In conclusion, the biogenic Te NRs were less toxic as compared to K2TeO3, and the no-observed-adverse-effect level (NOAEL) dose of Te NRs in 14 days subacute toxicity study was lower than 1.2 mg/kg.

The Effects of Methanolic Extract of Melissa officinalis on Experimental Gastric Ulcers in Rats.

BACKGROUND: Melissa officinalis (MO) has potent antioxidant activity. Recent research has demonstrated the anti-ulcer properties of some medicinal plants through their antioxidant properties. OBJECTIVES: The aim of this study was to evaluate the effects of methanolic extracts of MO on experimental gastric ulcers in rats. MATERIALS AND METHODS: Male Wistar rats (200 - 250 g) were starved for 24 hours prior to the induction of gastric ulceration by either indomethacin (48 mg/kg/oral) or water immersion restraint (WIR) stress. Experimental rats received either ranitidine (25 mg/kg) or MO extract (150, 300 and 450mg/kg) orally 2 hours prior to WIR stress or indomethacin treatment, for the evaluation of their gastroprotective effects. The control group received the same volume of saline. Gastric lesions were scored according to the surface of lesions on the ulcer index. Superoxide dismutase (SOD) and glutathione peroxidase (GPX) were determined as measures of antioxidant defense, and malondialdehyde (MDA) was determined to measure tissue oxidation. RESULTS: MO extract (150 and 300 mg/kg) significantly decreased the ulcer index in both the indomethacin (1.3 ± 0.09 and 1.5 ± 0.19, respectively) and WIR stress groups (1.5 ± 0.17 and 1.5 ± 0.22, respectively), as compared to the control rats (2.5 ± 0.28) (P < 0.01). MO extract (450 mg/kg) significantly reduced ulcer index readings in WIR stress rats (1.8 ± 0.31 vs. 2.4 ± 0.15 in the WIR group), however, MO extract at a dose of 450 mg/kg did not prevent indomethacin-induced gastric ulceration (2.4 ± 0.26). There was no significant difference in the ulcer index for MO extract- (150 and 300 mg/kg) and ranitidine-treated rats (P > 0.05). Also, MO extract (150 and 300 mg/kg) significantly reduced MDA serum levels (0.69 ± 0.6 µmol/L and 0.85 ± 0.24 µmol/L, respectively, vs. 4.5 ± 1.9 µmol/L in the saline group) and significantly increased antioxidants' SOD activities (296.3 ± 146.4 U/mL and 561.4 ± 120 U/mL, respectively, vs. 190.2 ± 63.8U/mL in the control group) and GPX levels (8273 ± 3049 U/mL and 14574 ± 5012 U/mL, respectively), compared to the control (3236 ± 1699 U/mL). CONCLUSIONS: Our results showed that MO extract may have a gastroprotective effect against experimental gastric ulcers in rats. The exact mechanism has not yet been determined, but it may be due to enhancing enzymatic antioxidant defenses and inhibiting lipid peroxidation.

Assessment of NAFLD cases and its correlation to BMI and metabolic syndrome in healthy blood donors in Kerman.

AIM: The aim of this study was to review cases of non-alcoholic fatty liver disease cases and to determine the prevalence of non-alcoholic fatty liver disease as a cause of elevated alanine aminotransferase in healthy blood donors in the Permian area and also assess risk factors of NAFLD such as BMI and correlation with metabolic syndrome in these subjects. BACKGROUND: Non-alcoholic fatty liver disease has been increasingly recognized as the most common pathological conditions affecting the liver. Non-alcoholic fatty liver disease is now recognized as the hepatic component of the metabolic syndrome, which includes hyperlipidemia, glucose intolerance, obesity, and systemic hypertension. PATIENTS AND METHODS: 2002 randomly selected blood donors were recruited for this study. Subjects with elevated serum ALT level (greater than two times the upper limit of normal) were chosen for further follow up. Subjects with a persistently elevated ALT level, evidence of steatosis on computerized tomography and a negative cirrhosis screen (viral hepatitis B and C serology, autoimmune hepatitis, transferrin saturation <45% and a no history of excess alcohol consumption or hepatotoxic medication) were presumed to have non-alcoholic fatty liver disease. RESULTS: 378 donors (20.5% of all subjects recruited) had elevated ALT levels at first measurement. 35 cases had persistently elevated serum ALT level. In 22 of these 35 cases (62.9%) non-alcoholic fatty liver disease was the diagnosis. The mean body mass index of the 22 cases was 31.18 ±5.7 and non-alcoholic fatty liver disease was associated with the metabolic syndrome in these subjects. CONCLUSION: Non-alcoholic fatty liver disease is the most common diagnosis for subjects with elevated serum ALT level in healthy blood donors in Kerman, Iran.