The Protective Effects of Pyridoxine on Linezolid-Induced Hematological Toxicity, Hepatotoxicity, and Oxidative Stress in Rats.

OBJECTIVE: Linezolid is often used to treat antibacterial-resistant infections. Linezolid can cause side effects. To date, the effectiveness of the simultaneous administration of pyridoxine and linezolid is unclear. Here we investigate the protective effect of pyridoxine on linezolid-induced hematological toxicity, hepatotoxicity, and oxidative stress in rats. MATERIAL AND METHODS: The 40 male pediatric Spraque-Dawley rats were separated into 4 groups: control, linezolid, pyridoxine, and linezolid-pyridoxine. A complete blood count, liver function test, and measurements of antioxidant enzyme activities for superoxide dismutase, glutathione peroxidase, catalase, and lipid peroxidation were performed in blood before treatment and 2 weeks after administration of the treatment. RESULTS: White blood cell and hemoglobin counts for the linezolid group decreased, and the alanine aminotransferase level in the linezolid group increased compared to their respective baseline values. Post-treatment white blood cell decreased in the linezolid and linezolid- pyridoxine groups compared to those in the control group (P < .001). Alanine aminotransferase levels increased in the linezolid and linezolid-pyridoxine groups compared to those in the control group (P < .001 and P < .05, respectively). The activity of superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde levels increased in the linezolid group compared to the control group (P < .001, P < .05, P < .001, and P < .001, respectively). Linezolid plus pyridoxine treatment caused a significant decrease in malondialdehyde levels and superoxide dismutase, catalase, and glutathione peroxidase enzyme activities compared to the linezolid group (P < .001, P < .01, P < .001, and P < .01, respectively). CONCLUSION: Pyridoxine may be an effective adjuvant agent for the prevention of linezolid toxicity in rat models.

The protective effect of Capparis ovata on 6-mercaptopurine-induced hepatotoxicity and oxidative stress in rats.

Capparis ovata is a member of Capparidacaeae family has been used in phytomedicine with a lot of positive effects such as an antioxidative, antihyperlipidemic, anti-inflammatory, and antihepatotoxic agent. The aim of this study was to research the protective effect of C. ovata on 6-mercaptopurine (6-MP) induced to hepatotoxicity and oxidative stress in rats. The rats were divided into 4 groups: control, 6-MP, C. ovataovate, and 6-MP + C. ovata. A complete blood count was performed, liver function test and antioxidant enzymes levels such as superoxide dismutase, glutathione peroxidase, catalase, and malondialdehyde were measured in blood before and after a 14-day test period. White blood cell and platelet counts were lower in the 6-MP group than other 3 groups (P < 0.005). Hepatic transaminase levels were higher in 6-MP group than the 3 groups (P < 0.05). Superoxide dismutase, glutathione peroxidase, and CAT levels were lower and malondialdehyde was higher in blood samples in 6-MP group than other 3 groups (P < 0.005). In conclusion, our tests were showed that C. ovata may be useful in patients receiving 6-MP therapy to prevent hepatotoxicity and in order to maintain uninterrupted therapy possibly reducing the risk of relapse. Although additional studies ensure that Capparis does not affect 6-MP antileukemic activity. We believe these results are important contribution to the literature.

Influence of hyperbaric oxygen therapy on central corneal thickness.

BACKGROUND/AIMS: Hyperbaric oxygen (HBO) therapy is used in the treatment of several disorders. Little is known about the effects of HBO treatment on corneal thickness. The aim of this study was to investigate the effect of HBO treatment on central corneal thickness. METHODS: Thirty-two subjects (18 males and 14 females, mean age 57.3 ± 16.7 years) undergoing HBO treatment were consecutively enrolled. The subjects were assigned into diabetic (n = 16) and nondiabetic groups (n = 16). Best-corrected visual acuity was recorded before HBO treatment, and anterior and posterior segment examinations were performed on a slit lamp biomicrosope. Central corneal thickness was measured with an ultrasonic pachymeter before and immediately after HBO treatment, which lasted 120 min at 2.4 atmospheres absolute with three 30-min oxygen and two 5-min air breathing periods. RESULTS: HBO treatment did not change the central corneal thickness in diabetic subjects (547.6 ± 34.5 vs. 548.6 ± 34.6 µm; p = 0.606). In nondiabetic subjects, however, the central corneal thickness was significantly reduced after HBO treatment (576.5 ± 34.8 vs. 569.0 ± 34.8 µm; p < 0.001). CONCLUSION: A single exposure to HBO treatment reduced the central corneal thickness in nondiabetic subjects but not in diabetic subjects. However, the change in central corneal thickness was minor.

Carbon monoxide-induced cortical visual loss: treatment with hyperbaric oxygen four years later.

OBJECTIVE: We present a patient who developed visual loss after carbon monoxide (CO) poisoning and was treated with hyperbaric oxygen. CLINICAL PRESENTATION AND INTERVENTION: A 21-year-old woman poisoned with CO (with coma lasting 4 h and carboxyhemoglobin level 46%) developed seizures and cortical blindness 3 days after poisoning. Four years later, her visual acuity was 0.2 in both eyes. An (18)F-fluorodeoxyglucose positron emission tomography (PET) scan showed reduced metabolism in the bilateral posterior temporal and occipital lobes. The patient received a total of 50 hyperbaric oxygen sessions over 3 months for visual loss and the visual acuity improved to 0.5 in both eyes. In addition, increased metabolism was detected in the brain in post-treatment PET scans. CONCLUSION: PET documented brain hypoperfusion 4 years after CO poisoning and hyperbaric oxygen therapy improved visual acuity. However, we cannot endorse routine use of hyperbaric oxygen for such patients, until results of further clinical trials demonstrate efficacy of hyperbaric oxygen in CO-induced chronic brain injury.

A novel antioxidant agent caffeic acid phenethyl ester prevents long-term mobile phone exposure-induced renal impairment in rat. Prognostic value of malondialdehyde, N-acetyl-beta-D-glucosaminidase and nitric oxide determination.

Caffeic acid phenethyl ester (CAPE), a flavonoid like compound, is one of the major components of honeybee propolis. It has been used in folk medicine for many years in Middle East countries. It was found to be a potent free radical scavenger and antioxidant recently. The aim of this study was to examine long-term applied 900 MHz emitting mobile phone-induced oxidative stress that promotes production of reactive oxygen species (ROS) and, was to investigate the role of CAPE on kidney tissue against the possible electromagnetic radiation (EMR)-induced renal impairment in rats. In particular, the ROS such as superoxide and nitric oxide (NO) may contribute to the pathophysiology of EMR-induced renal impairment. Malondialdehyde (MDA, an index of lipid peroxidation) levels, urinary N-acetyl-beta-D-glucosaminidase (NAG, a marker of renal tubular injury) and nitric oxide (NO, an oxidant product) levels were used as markers of oxidative stress-induced renal impairment and the success of CAPE treatment. The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in renal tissue were determined to evaluate the changes of antioxidant status. The rats used in the study were randomly grouped (10 each) as follows: i) Control group (without stress and EMR), ii) Sham-operated rats stayed without exposure to EMR (exposure device off), iii) Rats exposed to 900 MHz EMR (EMR group), and iv) A 900 MHz EMR exposed + CAPE treated group (EMR + CAPE group). In the EMR exposed group, while tissue MDA, NO levels and urinary NAG levels increased (p < 0.0001), the activities of SOD, CAT, and GSH-Px in renal tissue were reduced (p < 0.001). CAPE treatment reversed these effects as well (p < 0.0001, p < 0.001 respectively). In conclusion, the increase in NO and MDA levels of renal tissue, and in urinary NAG with the decrease in renal SOD, CAT, GSH-Px activities demonstrate the role of oxidative mechanisms in 900 MHz mobile phone-induced renal tissue damage, and CAPE, via its free radical scavenging and antioxidant properties, ameliorates oxidative renal damage. These results strongly suggest that CAPE exhibits a protective effect on mobile phone-induced and free radical mediated oxidative renal impairment in rats.