Possible protective effect of vitamin E on the joined cardio-renal effects of lead toxicity and noise stress in rats

Pollution is a worldwide problem and its potential to influence the physiological systems of human population is great. Many studies found that some pollutants have detrimental effects on human growth, particularly prenatal growth. Lead is one of the heavy metals commonly found in human populations. Lead toxicity was reported to be related to haemopoietic, hepatic, renal, nervous, gastrointestinal and reproductive disorders in man and animals. Recent studies have reported lead's potential for inducing oxidative stress which plays a role in the pathophysiology of lead toxicity. Noise stress from transportation sources also is related to different physiological effects on human, as well as impairment of auditory function and growth. Studies showed that combined exposure to noise and different pollutants affects heart and other organs. On the other hand, antioxidants were reported to reduce incidence to various physiological alterations accompanied by oxidative stress. Previous studies suggested that antioxidants may play an important role in abating some hazards of lead. The aim of the present work was to evaluate the possible ameliorating effect of vitamin E, as an antioxidant, on some alterations caused by lead or noise alone or in combination on kidney and heart biomarkers in adult male rats. Vitamin E was administered orally in a dose of 200 mg/kg two hours before lead dosage [15 mg/kg, i.p]. Animals were exposed to horn noise of about 110 dB for 30 minutes after administration of lead and/or vitamin E. The experiment was conducted for 14 consecutive days. The evaluated parameters included assessment of serum levels of urea, creatinine, Aspartate aminotransferase [AST], creatine kinase [CK] and lactate dehydrogenase [LDH] and levels of reduced glutathione [GSH] and malondialdehyde [MDA] in kidney and heart tissues. The histolopathological changes in both kidney and heart were reported. The obtained results revealed that lead and noise either alone or in combination caused statistically changes in the examined parameters with a good potential for vitamin E to protect against these changes

Evaluation of toxicity of boric acid in pregnant rats

Boron occurs most frequently in nature as borates and boric acid. Humans consume about a milligram of boron per day in foods such as fruit and vegetables. Boron is essential for the growth of many plants. At high doses, boron is developmentally toxic. The aim of this study was to evaluate signs of toxicity of boric acid administration in pregnant rats. Pregnant Sprague-Dawley rats were administrated oral doses 514, 257, 128, 51mg/kg of boric acid, from 7[th] to 16[th] day and from 1[st] to 20[th] day of gestation. Pregnant rats were evaluated for rate of abortion, weight gain during pregnancy and relative weights of liver, kidneys, placenta and uteri. At 20[th] day. The animals were sacrificed and histological study of liver and kidneys were done . Results showed that the rate of abortion was increased with the high doses meanwhile the weight gain of pregnant rats was decreased, moreover ,the relative weights of liver and kidneys of pregnant rats were increased and the weight of placenta and uteri were decreased in treated groups as compared to control . Histopathological studies of liver and kidneys revealed signs of toxicity in the form of congestion of blood vessels and fatty degeneration with atrophic changes in the parenchyma's cells of liver and kidneys. In conclusion, boric acid administration in pregnant rats induced toxicities in the form of enhanced rate of abortion ,decreased weight gain during pregnancy .Hepatic and renal toxicities of boric acid were confirmed by histopathological abnormalities. Boric acid toxicity in pregnant rats was dose and time dependent

Evaluation of the protective effect of thyme oil on possible toxicity of vinerlbine [navelbine] in mice

Vinorelbine [Navelbine] is a semi-synthetic vinca alkaloid derived from vinblastine which is used mainly to treat non-small cell lung cancer. One of the most recognized natural antioxidant is Thymus vulgaris which plays an important role in the chemoprevention of diseases. The aim of this study was to evaluate the possible hematological, kidney and lung toxicities of Navelbine in albino mice and to clarify the protective effects of Thyme oil when co-administrated with Navelbine. Eighty Male albino mice were divided into four groups: normal control group, Navelbine treated group, Thyme oil treated group and Navelbine-Thyme oil treated group. Navelbine was injected intraperitoneal in mice in a dose of 10mg/kg/week for four weeks. Thyme oil was administered by gavage in a dose of 72 micro g/mice every second day for twenty days. Parameters done included: complete blood picture, kidney function tests [blood urea and serum creatinine], albumin and total protein were measured. Histological analysis was conducted on tissues collected from kidney and lung of normal and treated groups. Results of this study showed that Navelbine caused mild to moderate anemia, significant leucopenia with relative lymphocytosis and thrombocytopenia. Navelbine induced mild renal toxicity in the form of increase in blood urea and serum creatinine. Serum total proteins and albumin were decreased. Histopathological changes observed in the mice kidney were in the form of heavy lymphocytic infiltrations, oedema in the glomeruli and congested blood vessels. Pulmonary histopathology showed congestion, distorted alveoli, mononuclear cells infiltrations, interseptal oedema and hyperplasia of the bronchiolar epithelial cells. By co-administration of Thyme oil improvement of haematological and biochemical parameters had occurred meanwhile mild changes had occurred on histological studies. In conclusion, Thyme oil could be used as a chemoprotective agent against Navelbine induced toxicity in albino mice

Developmental toxicity of boric acid in rats' fetuses

Boric acid [BA], an essential plant micronutrient, occurs naturally in fruits and vegetables. Boric acid has been shown to cause developmental abnormalities in the fetuses of pregnant rats. The present study examined its effects on the development of rat fetuses. Boric acid was orally administrated to pregnant rats by gastric intubation 514, 257, 128, 51 mg/kg, from the 7[th] to 16[th] of gestation and from the 1[st] to 20[th] day of gestation. Boric acid has been shown to induce fetal growth retardation and increased fetal mortality rate. The morphological examination of the fetuses revealed anomalies of limbs [paralysis, adactyly and brachdactyly] and external hematomas. Fetal skeletal staining showed delayed ossification of central and peripheral skeletons with obvious abnormalities of the terminal ribs in the form of shortness, agenesis and wavy ribs. Histopathological examination of liver and kidneys revealed signs of toxicity in the form of congestion of blood vessels and fatty and hydropic degeneration with atrophic changes in the hepatic and renal cells. In conclusion, prenatal boric acid induced developmental fetal toxicity in the form of intrauterine growth retardation with delayed ossification of bones, hepatic and renal histopathological changes. The induced abnormalities of boric acid on the fetus were dose and time dependent

study on the possible acute toxic interactions between digoxin and some cardiac drugs in mice

Digoxin-drug interactions are relatively common causes of digitalis toxicity. Cardiac patients receiving digoxin therapy are particularly prone to interactions with commonly co-administered medications such as amiodarone [antiarrhythmic] and nimodipine [calcium channel blocker].The aim of this study was to estimate intraperitoneal LD[50] of digoxin, nimodipine and amiodarone in male mice and to detect acute toxic interactions that could occur between digoxin and either nimodipine or amiodarone. It was concluded that LD[50] of digoxin, nimodipine and amiodarone were equal to 3.25 mg/kg, 13.2 mg/kg and 625 mg/kg respectively. Co-administration of LD[50], of digoxin with 1/4, 1/2 and I of LD[50] of nimodipine, reduced acute toxicity to 33%, 67% and 75% respectively. Meanwhile co-administration of digoxin with amiodarone produced acute toxicity equal to 75%, 100% and 100% respectively. A beneficial antagonistic toxic interaction had occurred on concomitant intraperitoneal administration of digoxin and nimodipine in mice meanwhile a synergistic toxic interaction had occurred between digoxin and amiodarone

study on acute and sub-acute toxicity of cefepime in mice

Cefepime is a fourth generation cephalosporin used mainly for treatment of lower respiratory tract, intra-abdominal and urinary tract infections In this study, acute toxicity of cefepime was done in mice and LD5O was calculated .Sub-acute toxicity was evaluated in mice by daily intraperitoneal administration of cefepime for 14 days in a dose equal to 500mg/kg. Kidney functions [blood urea and serum creatinine levels] and liver enzyme [serum ALT level] were estimated at the end of 14 days and after stoppage of cefepime by 2 weeks. Histopathological studies of livers and kidneys were done at the same previous periods. It was concluded that LD50 of cefepime in mice was equal to 6250 mg/kg by intraperitoneal route .Cefepime 500mg/kg, was well tolerated in mice with 100% survival rate. Mild transient elevations of ALT, urea and creatinine had occurred after treatment for 14 days. Minor histopathological changes had occurred in livers and kidneys