Long-term pulmonary histopathologic changes in rats following acute experimental exposure to chlorine gas

In this study, we aimed to investigate the long-term histopathologic changes in the lungs of rats exposed to a high concentration of chlorine gas. Twenty-four Sprague-Dawley rats were divided into three groups: the control group (group I) (n = 8), early-examined group (group II) (n = 8), and late-examined group (group III) (n = 8). In group II the lungs of rats were taken out just after the exposure, whereas in group III the lungs were taken out 45 days after the exposure. Eosinophilic liquid accumulation in alveoli and bronchi, diffuse intraalveolar edema, vascular congestion, severe perivascular edema, and free bleeding in intraalveolar and interstitial area were observed in the lungs of rats in group II. Interstitial fibrosis and thickening of the alveolar septa were observed in group III. These findings suggest that the people using these cleaning agents are at risk of harming themselves, and the victims of chlorine gas injury should be reexamined at a later period since they may have pulmonary damage even after 45 days of exposure.     

The Effect of Nebulized NaHCO3 Treatment on “RADS” Due to Chlorine Gas Inhalation

Chlorine is one of the most common substances involved in toxic inhalation. As with all irritant gases, the airway injuries caused by chlorine gas may result in clinical manifestations similar to those of asthma. In this study, we investigated the effect of nebulized sodium bicarbonate (NSB) on the treatment and quality of life (QoL) of victims exposed to chlorine gas. Forty-four consecutive patients with reactive airways dysfunction syndrome (RADS) due to chlorine inhalation (40 females and 4 males, age range 17–56 yr) were included in this study. Patients were placed in control and treatment groups in a sequential odd–even fashion based on their order of presentation. Treatment of all patients included corticosteroids and nebulized short-acting β2-agonists. Then the control group (n = 22) received nebulized placebo (NP), and the NSB group (n = 22) received NSB treatment (4 cm³ of 4.20% sodium bicarbonate solution). A quality of life (QoL) questionnaire and pulmonary function tests (PFTs) were performed before and after treatments in both groups. The most common symptoms were dyspnea (82%) and chest tightness (82%). Baseline characteristics of both groups were similar. Compared to the placebo group, the NSB group had significantly higher FEV1 values at 120 and 240 min (p < .05). Significantly more improvement in QoL questionnaire scores occurred in the NSB group compared to the NP group (p < .001). Thus, NSB is a clinically useful treatment, as tested by PFTs and QoL questionnaire, for patients with RADS caused by exposure to chlorine gas.     

Surgical treatment of hepatocellular carcinoma with cirrhotic esophageal varices and hypersplenism:a 184 case report

In treating hepatocellular carcinoma (HCC) patients with advanced cirrhosis, one of the most difficult problems is concomitant esophageal varices and hypersplenism. Whether these conditions should be treated surgically in association with HCC resection is still in debate. To elucidate whether esophageal devascularization or splenectomy is beneficial when simultaneously performed with liver resection in HCC patients with both varices and hypersplenism, HCC patients (n = 184) with esophageal varices and hypersplenism received one of the three treatments: simultaneous liver resection and esophageal devascularization (Group I, n = 41); simultaneous liver resection and splenectomy (Group II, n = 61); liver resection only (Group III, n = 82). The incidences of postoperative complications of the three groups were 31.7%, 29.5% and 24.4%, respectively, with no significant difference among them. The 5-year tumor-free survival rates for the group I, group II and group III were 34.1%, 36.1% and 37.8%, respectively. Variceal bleeding caused death by only 4.2% in group I, but by 14.3% in group II and 23.2% in group III. The survival rates in the group I and the group II were comparable to those in the group III, however, the recurrences of postoperative fatal variceal bleeding in group I and group II were significantly lower than those in group III. The results suggest that HCC patients with esophageal varices and hypersplenism should undergo hepatic resection plus esophageal devascularization or splenectomy if radical resection of HCC can be expected.     

Changes in urinaryn-hexane metabolites by co-exposure to various concentrations of methyl ethyl ketone and fixedn-hexane levels

To make clear how then-hexane metabolism is modified by co-exposure with MEK, rats were exposed to various concentrations of MEK mixed with a fixed concentration ofn-hexane. Twenty-four male Wistar rats were divided into four equal groups. Each group was exposed for 8 h to 2000 ppmn-hexane, 2000 ppmn-hexane plus 200 ppm MEK, 2000 ppmn-hexane plus 630 ppm MEK and 2000 ppmn-hexane plus 2000 ppm MEK, respectively. Free metabolites and the sum of free and conjugated metabolites ofn-hexane were analyzed by gas chromatography. The main metabolite was 2-hexanol during the exposure and 2,5-hexanedione (2,5-HD) after the exposure in any group. The main metabolites, 2-hexanol and 2,5 HD, decreased in iverse proportion to the co-exposed MEK concentrations. The results suggest that augmentation ofn-hexane neurotoxicity by MEK co-exposure could not be explained only by 2,5-HD. In addition, 2,5-HD is recommended as an index for biological monitoring ofn-hexane exposure. However, one should be careful to evaluate the exposedn-hexane concentration by urinary 2,5-HD, becausen-hexane metabolism could be largely modified by co-exposure with MEK.     

Ciclosporin metabolite pattern in blood and urine of kidney graft patients in relation to liver function

Summary Ciclosporin, an immunosuppressant, is metabolized by the liver cytochrome P450 system. Changes in the pattern of its metabolites in blood and urine in patients with disturbed liver function have been studied.Forty seven kidney graft patients receiving 2.9 mg/kg/d ciclosporin b.i.d., and no additional medication that would interfere with ciclosporin metabolism, were allocated to three groups according to liver function: I with normal liver function (n=19), II with elevated liver enzyme activity or bilirubin concentration in serum (n=20), and III with cholestasis (n=8). Ciclosporin and 17 metabolites were determined in blood and 24 h-urine.In blood the trough concentrations of metabolites M19 and M1A were significantly higher in group III than in groups I and II. The total quantity of metabolites excreted in 24 h-urine was significantly different for H230, M4N69 and M1A (group III>I=II). Renal excretion of the daily dose of ciclosporin in patients in group I was 2.7%, group II 3% and group III 5.7%. In group III compared to group I the ciclosporin metabolite pattern was shifted to a relatively higher concentration of M19 in blood and of H 230, M19 and M1A in urine.Since high ciclosporin metabolite concentrations appear to be associated with nephrotoxicity, the metabolite pattern in patients with impaired liver function should be monitored.     

Oxygen toxicity: Protection of the lung by bacterial lipopolysaccharide (endotoxin)

Adult rats were exposed to > 95% O₂ for a 72-hr period and treated with small dosages of endotoxin (250 μg/kg/day, 1/100th LD50) during the exposure or with a single dose of endotoxin (500 μg/kg) administered just prior to the hyperoxic exposure. Endotoxin treatment increased the survival rate in hyperoxia from 12/44 (27%) for untreated rats to 38/40 (95%) for the treated animals (p < 0.05). In addition, the endotoxin-treated animals had significantly decreased O₂-induced pulmonary edema and pleural fluid accumulation compared to the untreated rats (p < 0.05). Histological examination by light microscopy demonstrated marked lung damage in the untreated. hyperoxia-exposed animal lungs (perivascular, interstitial, and alveolar edema and lung hemorrhage) but only minimal changes in the lungs of the endotoxin-treated group of animals exposed to hyperoxia. Transmission electron microscopy showed a protective action of endotoxin treatment on the pulmonary capillary endothelium, compatible with the decreased exudative changes (edema) observed in the O₂-exposed endotoxin-treated lungs. Indomethacin and methylprednisolone pretreatment failed to alter the protective action of endotoxin versus pulmonary O₂ toxicity.     

Tumor necrosis factor-α induced protein 6 attenuates acute lung injury following paraquat exposure

Context: Paraquat exposure commonly occurs in the developing countries and the mortality rate is high. However, there is currently no consensus on the efficacy of treatment for paraquat exposure.

Objective: The study was aimed to explore the effects of tumor necrosis factor-α (TNF-α) induced protein 6 (TSG-6) on acute lung injury (ALI) following paraquat exposure in rats.

Materials and methods: Male Sprague–Dawley (SD) rats were randomly divided into the sham group (n?=?8), the paraquat group (n?=?8), and the paraquat TSG-6-treated group (n?=?8). Rats were administered with 50?mg/kg of paraquat intraperitoneally. At 1?h after exposure, rats were treated with 30?μg of recombinant human TSG-6 (rhTSG-6) intraperitoneally. After 6?h of exposure, ALI scores were evaluated by histology and the expression of pro-inflammatory cytokines in lung was assayed using real-time RT-PCR.

Results: ALI scores were significantly lower in the paraquat TSG-6-treated group, compared with the paraquat group (p?<?0.05). The expression of interleukin (IL)-1β, IL-6, and TNF-α mRNA was significantly lower in the paraquat TSG-6-treated group, compared with the paraquat group (p?<?0.01, respectively).

Discussion and conclusion: Administration of rhTSG-6 attenuates ALI following paraquat exposure by suppressing inflammatory response.     

Two-week aerosol inhalation study in rats of ethylene oxide/propylene oxide copolymers.

Previous studies have shown that aerosols of an ethylene oxide/propylene oxide copolymer (UCON 50-HB-5100) produced an inflammatory response in lungs of rats in short-term repeated exposures at relatively low concentrations. This study was carried out on related polyalkylene glycols (EO/PO copolymers) to determine if similar effects would occur upon short-term repeated exposure. Rats were treated by whole body liquid droplet aerosol exposures of six hours per day, five days per week for two consecutive weeks to each of five EO/PO copolymers. The exposure level for the positive control (UCON 50-HB-5100) was 55 mg/m3, while the remaining 4 test copolymers were evaluated at 100 mg/m3. Each exposure group consisted of ten male albino rats. After three exposures, nine of ten rats exposed to UCON 50-HB-5100, and six of ten rats exposed to UCON 50-HB-2000 had died. At necropsy, congestion, consolidation and red discoloration of the lungs were noted. A moderate to severe alveolitis, characterized by intraalveolar edema, hemorrhage and fibrin deposition, was observed after five days of exposure. At necropsy, these rats exhibited elevated lung weights and similar macroscopic and microscopic lesions. Rats exposed to the other test materials (UCON 75-H-1400, Pluronic L17R1, Pluronic L31, and Pluronic L64) survived with essentially no signs of toxicity through the ten exposure days. Body weights, organ weights, hematological evaluation, pharmacotoxic signs, and macroscopic and microscopic evaluation after necropsy were similar between groups and when compared to the negative control group. Only a slight alveolitis was noted after two weeks of exposure which subsided by two-weeks post exposure.     

Correlative investigation of copper/low-density polyethylene nanocomposite on the endometrial angiogenesis in rats

The purpose of this study was to investigate the effects of copper/low-density polyethylene nanocomposite (nano-Cu/LDPE) on the endometrial angiogenesis in rats, and 100 sexual mature female SD rats were randomly divided into five groups: sham-operation groups (SO group, n = 20), bulk copper groups (Cu group, n = 20), LDPE groups (n = 20), nano-Cu/LDPE groups I (n = 20) and II (n = 20). The levels of angiopoietin-2 (Ang-2), its receptor (Tie-2) and CD34 of the rats’ endometria in each group were examined by using the S-P method of the immunohistochemistry 30 and 180 days after insertion, respectively. Compared with those in the SO group, the expression of Ang-2 and Tie-2 in all the experimental groups was obviously increased 30 days after insertion, and these parameters in nano-Cu/LDPE groups, except for Ang-2 level in nano-Cu/LDPE group II, were significantly lower in comparison with those in Cu group (P < 0.05). On the 180th day after insertion, Ang-2 and Tie-2 levels were still higher in Cu group and LDPE group, but there was no difference of Ang-2 and Tie-2 levels between nano-Cu/LDPE groups and the SO group (P > 0.05). Compared with those in the SO group, the significant increases in microvessel density (MVD) were observed on the 30th and the 180th day after the insertion of the bulk copper (P < 0.05). There was no significant difference in MVD counts before and after the insertion of nano-Cu/LDPE (P > 0.05). The results show that Nano-Cu/LDPE have slighter influence on the endometrial angiogenesis than bulk copper.     

The effects of exercise following exposure to bis(trifluoromethyl) disulfide.

Bis(trifluoromethyl) disulfide (TFD) was originally designed for use as an agricultural fumigant. Inhalation of toxic doses of TFD results in varying degrees of pulmonary edema. The purpose of this study was to determine if exhaustive exercise would potentiate the toxic effects of TFD. One group of treadmill-acclimated rats was exercised to exhaustion following a 10-minute whole-body exposure to TFD. A second group was similarly exposed but not exercised. Two other groups of rats were sham exposed; one was exercised while one remained sedentary following the sham exposure. Twenty-four hours after exposure, the animals were sacrificed; the lungs were removed and weighed, and a portion was collected for histopathologic examination. The remaining lung tissue was allowed to dry to constant weight. There was no difference in endurance times between exposed and sham-exposed rats. There was a significant increase in the amount of pulmonary edema and associated pulmonary pathology in rats exercised following exposure to TFD. Eleven of twelve animals exercised following exposure to TFD and three of twelve animals which remained sedentary following exposure died by 24 hours. The degree of pulmonary pathology in all rats exposed to TFD was profound.     

Cardioprotective effects of rosuvastatin and carvedilol on delayed cardiotoxicity of doxorubicin in rats

Context: Doxorubicin is widely used anti-neoplastic drug but has serious cardiotoxicity. Long-term cardioprotective effects of statin and carvedilol against delayed cardiotoxicity of doxorubicin was not well elucidated.

Objective: To evaluate long-term cardioprotective effects of co-administered rosuvastatin and carvedilol against chronic doxorubicin-induced cardiomyopathy (DIC) in rats.

Methods: Sixty-one rats were assigned to six groups: group I, control; group II, doxorubicin only (1.25 mg/kg, bi-daily, I.P.); group III, doxorubicin + rosuvastatin (2 mg/kg/day, P.O.); group IV, doxorubicin + rosuvastatin(10 mg/kg/day, P.O.); group V, doxorubicin + carvedilol (5 mg/kg/day, P.O.); group VI, doxorubicin + carvedilol (10 mg/kg/day, P.O.). Drugs were administered for 4 weeks (by week 4) and rats were observed without drugs for 4 weeks (by week 8).

Results: After 4 weeks discontinuation of drugs (week 8), group III showed higher +dP/dt (p = 0.058), lower ?dP/dt (p = 0.009), lower left ventricular (LV) tissue malondialdehyde (MDA; p = 0.022), and less LV fibrosis (p = 0.011) than group II. Group IV showed similar results to group III. However, in group V and VI, carvedilol failed to reduce LV dysfunction, elevation of troponin or myocardial fibrosis, although group V showed lower LV tissue MDA (p = 0.004) than group II.

Discussion and conclusions: Myocardial injury and LV systolic/diastolic dysfunction at week 8 was alleviated by co-administered rosuvastatin, but not by carvedilol. It is unclear whether the cardioprotective effect of rosuvastatin is attributed to a suppression of oxidative stress induced by doxorubicin, because carvedilol did not exhibit a cardioprotective effect despite its antioxidant effects.     

Effects of Exercise Following Exposure to Perfluoroisobutylene

Abstract

Perfluoroisobutylene (PFIB) is a toxic chemical encountered in industry as a pyrolysis product of tetrafluoroethylene polymers, such as Teflon. Inhalation of toxic doses of PFIB results in varying degrees of pulmonary edema. The purpose of this study was to determine if exhaustive exercise would potentiate the toxic effects of PFIB. One group of treadmill-acclimated rats was exercised to exhaustion following a lhnin whole-body exposure to PFIB (approximately 0.75 × LCt50). A second group was similarly exposed but not exercised. Two other groups of rats were sham exposed; one was exercised while one remained sedentary following the sham exposure. Twenty-four hours after exposure, the animals were sacrificed; the lungs were removed and weighed, and a portion was collected for histopathologic examination. The remaining lung tissue was allowed to dry to constant weight. There was a significant increase in the amount of pulmonary edema and associated pulmonary pathology in rats exercised following exposure to PFIB. Exposure to this concentration of PFIB caused no decrement in immediate postexposure endurance. The degree of pulmonary pathology in all rats exposed to PFIB was profound.     

Assessment of early acute lung injury in rodents exposed to phosgene

Phosgene is a highly reactive oxidant gas used in the chemical industry. Phosgene can cause life-threatening pulmonary edema by reacting with peripheral lung compartment tissue components. Clinical evidence of edema is not usually apparent until well after the initial exposure. This study was designed to investigate early signs of acute lung injury in rodents within 45–60 min after the start of exposure. Male mice, rats, or guinea pigs were exposed to 87 mg/m³ (22 ppm) phosgene or filtered room air for 20 min followed by room air washout for 5 min. This concentration-time exposure causes a doubling of lung wet weight within 5 h. After exposure, animals were immediately anesthetized i.p., with pentobarbital. Bronchoalveolar lavage (BAL) was performed and fluid analyzed for total glutathione (GSH), lipid peroxidation thiobarbituric acid reactive substances (TBARS), and protein concentration. Lungs were perfused with saline to remove blood, freeze-snapped in liquid N₂, analyzed for tissue GSH, and TBARS. Lung edema was assessed gravimetrically by measuring tissue wet/dry (W/D) weight ratios and tissue wet weights (TWW). W/D and TWW were significantly higher in mice for phosgene vs air (P=0.001, P<0.0001, respectively), but not in rats or guinea pigs. Tissue TBARS was significantly higher in phosgene-exposed guinea pigs, P=0.027; however, BAL TBARS was higher in both rats and guinea pigs, P=0.013 and P=0.006, respectively. Tissue GSH was significantly lower in phosgene-exposed rats and guinea pigs but not mice, whereas BAL GSH was higher in rats, P<0.0001. There were significantly higher BAL protein levels in all phosgene-exposed species: mice, P<0.0001; rats, P<0.0001; and guinea pigs, P=0.002. Although there appears to be a species-specific biochemical effect of phosgene exposure for some biochemical indices, measurement of BAL protein in all three species is a better indicator of ensuing edema formation. Received: 30 June 1997 / Accepted: 5 January 1998     

Two-Year Inhalation Exposure of Female and Male B6C3F1 Mice and F344 Rats to Chlorine Gas Induces Lesions Confined to the Nose

Chlorine gas is a respiratory irritant in both animals and humansthat produces concentration-dependent responses ranging fromminor irritation to death. Female and male B6C3F1 mice and F344rats were exposed to chlorine gas for up to 2 years to determinechronic toxicity and carcinogenicity. Groups of approximately70 each of female and male mice and rats were exposed to 0,0.4, 1.0, or 2.5 ppm chlorine gas for 6 hr/day, 5 days/week(mice and male rats), or 3 alternate days/week (female rats)for 2 years, with an interim necropsy of rats at 12 months (10rats/sex/concentration group). A complete necropsy was performedon all animals. Histological examination was performed on allorgans from high-concentration and control animals and selectedtarget organs from mid-and low-concentration groups. Exposure-dependentlesions were confined to the nasal passages in all sex and speciesgroups. Chlorine-induced lesions, which were most severe inthe anterior nasal cavity, included respiratory and olfactoryepithelial degeneration, septal fenestration, mucosal inflammation,respiratory epithelial hyperplasia, squamous metaplasia andgoblet cell hypertrophy and hyperplasia, and secretory metaplasiaof the transitional epithelium of the lateral meatus. Intracellularaccumulation of eosinophilic proteinaceous material was alsoa prominent response involving the respiratory, transitional,and olfactory epithelia, and in some cases the squamous epitheliumof the nasal vestibule. Many of these nasal lesions exhibitedan increase in incidence and/or severity that was related tochlorine exposure concentration and were statistically significantlyincreased at all chlorine concentrations studied. Male miceand female rats appeared more sensitive to chlorine than femalemice and male rats, respectively. The reasons for the sex differenceswithin a species were not determined. Interspecies differencesin regional dosimetry and site-specific tissue susceptibilityto chlorine exposure should be taken into account when usingthese data for accurate assessment of potential human healthrisks. The incidence of neoplasia was not increased by exposure,indicating that inhaled chlorine in rats and mice is an upperrespiratory tract toxicant but not a carcinogen.     

Nicotine and vascular endothelial dysfunction in female ovariectomized rats: role of estrogen replacement therapy

Objectives The protective effects of estrogen replacement therapy (ERT) against oxidative injury and endothelial dysfunction in the aortic tissues induced with nicotine in ovariectomized (OVX) rats were investigated. Methods Female rats were divided into a sham‐operated group (n = 8) and four groups in which OVX rats received either vehicle (0.1 ml sesame oil, i.m., n = 8), or nicotine (0.1 mg/kg, s.c., n = 8), or estradiol benzoate (0.1 mg/kg, i.m., n = 8), or both nicotine and estradiol benzoate (n = 8) starting at week 5 after the surgery and continuing for the following 6 weeks. Key findings ERT was effective in preventing the rise in plasma lipid profile, atherogenic index and the level of induced endothelin‐1 (ET‐1) in nicotine‐treated OVX rats. It also reduced aortic malondialdehyde, hydroxyproline levels, calcium content and caspase‐3 expression induced in nicotine‐treated OVX rats. ERT increased serum estradiol, high‐density lipoprotein cholesterol and nitric oxide levels in nicotine‐treated OVX rats. Furthermore, ERT was effective in restoring reduced glutathione and cyclic guanosine monophosphate contents and endothelial nitric oxide synthase expression in aortic tissues of nicotine‐treated OVX rats. Conclusions Short‐term ERT could be a promising therapeutic strategy to minimize nicotine‐induced oxidative stress and vascular endothelial dysfunction in menopausal women subjected to environmental smoke.     

全氟异丁烯单次暴露诱发小鼠急性肺损伤的长期效应

目的 探讨全氟异丁烯( PFIB)单次暴露诱发急性肺损伤的长期效应.方法 70只雄性小鼠暴露于全氟异丁烯130 mg·m-3 5 min.10只小鼠于暴露后24 h评价肺水肿程度.其余小鼠分别在PFIB暴露后2,4,6,8,12和16周,应用HE染色和天狼星红染色分别观察肺组织的病理变化和胶原沉积,测定肺及血浆中羟脯氨...     

The relevance of 4,5-dihydroxy-2-hexanone in the excretion kinetics ofn-hexane metabolites in rat and man

Male Wistar rats were exposed ton-hexane concentrations between 50 and 3000 ppm for 8 h, and urinary excretion kinetics of then-hexane metabolites 1-hexanol, 2-hexanol, 3-hexanol, 2-hexanone, 2,5-hexanedione, and 4,5-dihydroxy-2-hexanone were assessed. The amounts of metabolites excreted were linearly dependent on then-hexane exposure concentration, up to an exposure of about 300 ppm. Above 300 ppm exposure the metabolite excretion indicated saturation kinetics in the metabolism ofn-hexane. In its quantity, the newly described 4,5-dihydroxy-2-hexanone was the second metabolite, its amount in the urine being about ten times higher than that of excreted 2,5-hexanedione. Using gas chromatography-mass spectrometry the occurrence of 4,5-dihydroxy-2-hexanone as ann-hexane metabolite in urine of man was confirmed after exposure of a male volunteer to a mean of 217 ppmn-hexane for 4 h (laboratory exposure). Twenty-six hours after starting this exposure the excretion of 4,5-dihydroxy-2-hexanone (as a result of then-hexane exposure) reached a level which was four times higher than the excretion of 2,5-hexanedione. The results in both rat and man indicate the relevance of 4,5-dihydroxy-2-hexanone as a metabolite ofn-hexane metabolism. Formation of this metabolite may be viewed as a route of detoxification.     

Comparison of Fetotoxic Effects of a Dermally Applied Complex Organic Mixture in Rats and Mice

A high-boiling (288–454?C), coal-derived complex organicmixture (COM) has been shown to be teratogenic in rats followinginhalation and oral routes of exposure. To determine whethersimilar changes also occur after dermal exposure to this COM,pregnant rats and mice were exposed during periods of organogenesis(Days 11 to 15 of gestation). Shaved backs were painted with0, 500, or 1500 mg/kg of the COM (control, low, or high dose,respectively); the exposed area was not occluded. Maternal weightgain during the gestation period decreased with increasing dosein rats but not in mice. Examination of rat fetuses on Day 20of gestation showed that resorptions had occurred in more than90% of low-and high-dose litters (vs 6% in the control group).In mice, fetal examinations on Day 18 of gestation showed thatresorptions occurred in 71% of litters from both exposure groups(vs 14% in the controls). Fetal measurements indicated thatboth the weight and the length of rat fetuses decreased withincreasing dose, but mouse fetuses were unaffected. Cleft palates,absent in the control groups, were observed in 50 to 55% ofthe high-dose group and 5 to 8% of the low-dose fetuses of bothspecies. Small fetal lungs occurred in nearly 100% of the exposedrat fetuses and in 25% of the high-dose mice; the incidenceof small lungs was 1% in control animals. Other variations observedin exposed groups included edema and reduced ossification inthe rat and renal pelvic cavitation in the mouse. In conclusion,dermal exposure of dams to COM resulted in life-threateningmorphological alterations in fetuses of both species similarto those seen following exposure by Other routes.     

Effects of third generation mobile phone-emitted electromagnetic radiation on oxidative stress parameters in eye tissue and blood of rats

Purpose: To investigate the effects of electromagnetic radiation (EMR) emitted by a third generation (3G) mobile phone on the antioxidant and oxidative stress parameters in eye tissue and blood of rats.

Methods: Eighteen Wistar albino rats were randomly assigned into two groups: Group I (n = 9) received a standardized a daily dose of 3G mobile phone EMR for 20 days, and Group II served as the control group (n = 9), receiving no exposure to EMR. Glutathione peroxidase (GSH-Px) and catalase (CAT) levels were measured in eye tissues; in addition, malondialdehyde (MDA) and reduced GSH levels were measured in blood.

Results: There was no significant difference between groups in GSH-Px (p = 0.99) and CAT (p = 0.18) activity in eye tissue. There was no significant difference between groups in MDA (p = 0.69) and GSH levels (p = 0.83) in blood.

Conclusions: The results of this study suggest that under a short period of exposure, 3G mobile phone radiation does not lead to harmful effects on eye tissue and blood in rats.     

Effects of MEK on kinetics ofn-hexane metabolites in serum

The neurotoxicity ofn-hexane is thought to be caused ultimately by 2,5-hexanedione (2,5-HD), one of then-hexane metabolites. The potentiation ofn-hexane neurotoxicity by co-exposure with MEK, therefore, is suspected to be related to kinetics of 2,5-HD in blood. To clarify the kinetics ofn-hexane metabolites in the mixed exposure ofn-hexane and MEK, rats were exposed to 2000 ppmn-hexane or a mixture of 2000 ppmn-hexane and 2000 ppm MEK, and the time courses of serumn-hexane metabolites were determined. 2,5-HD in serum increased until 2 h after the end of exposure, when serum 2,5-HD concentration reached a peak of 16.35 g/ml in then-hexane-alone group. In contrast, 2,5-HD in the mixed exposure group increased much more slowly during and after exposure than in then-hexane-alone group. It reached a peak of 2.12 g/ml at 8 h after the end of exposure. Serum MBK, a precursor of 2,5-HD in the co-exposure group, was about half in then-hexane-alone group during exposure. However, MBK decreased more slowly in the co-exposure group than in then-hexane-alone group after the end of the exposure. The results suggest that co-exposed MEK might inhibit oxidation ofn-hexane and decrease clearance ofn-hexane metabolites. Co-exposed MEK did not increase serum 2,5-HD, which was considered a main neurotoxic metabolite. Therefore the enhancement of neurotoxicity could not be attributed to increased serum 2,5-HD in the co-exposed group. The mechanism of enhancement of neurotoxicity ofn-hexane by MEK should be studied further.