Study on the In Vitro Effects of the Mixtures of Polycyclic Aromatic Hydrocarbons (PAHs) and Heavy Metals on Ethoxyresorufin-O-Deethylase (EROD) Activity in Mossambica tilapia Liver

This paper reports in vitro effects of individual heavy metals (Cd²⁺, Cu²⁺ and Hg²⁺), and PAHs, including benzo[a]pyrene(BaP), indeno[1,2,3-cd]pyrene (IP) and fluoranthene (FL), and their mixtures on ethoxyresorufin-O-deethylase (EROD) activities using a plate-reader method. The results showed that all three metals inhibited EROD activity, while BaP/IP significantly induced the enzyme. However, FL alone decreased EROD activity. Moreover, co-treatment with BaP/IP and heavy metals inhibited PAH-induced EROD activities, while combined exposure to FL and heavy metals induced FL-inhibited EROD activities.     

Cytological changes in association with ethoxyresorufin o-deethylase induction in fish upon dietary exposure to benzo[a]pyrene

Juvenile areolated grouper (Epinephelus areolatus) were exposed to two levels of dietary benzo[a]pyrene (BaP; 0.25-12.5 microg/g body wt/d) for four weeks, followed by four weeks of depuration. Significant increase in hepatic ethoxyresorufin O-deethylase (EROD) activities was found after one week, preceding an increase in lipopigments (as measured by quantitative transmission electron microscopy) in week 2 of exposure. The EROD activities in the BaP-treated fish subsided at week 4 of exposure and throughout the depuration period. Lipopigments in the high-dose group appeared to be more persistent than that of the EROD activity during the exposure period and remained significantly higher than that of the controls at week 4. Levels of lipopigments, however, rapidly subsided on withdrawal of BaP exposure. These results appear to suggest that changes in EROD activities would precede cytological changes and that both the observed cytological and biochemical changes are reversible. Results of the present study also lend further support to our earlier findings on Solea ovata, that a significant relationship exists between EROD activity and lipopigment accumulation (as measured by volume density, absolute volume, numerical density, and absolute density; r = 0.483-0.358, p < 0.05), regardless of fish species (S. ovata and aerolated grouper) as well as the routes of exposure to BaP (intraperitoneal injection or dietary exposure). This provides strong supporting evidence that elevated EROD activities in fish liver do not merely indicate exposure to polyaromatic hydrocarbons (PAHs) but are also associated with significant biological effects. Our results showed that hepatic EROD activity and lipopigments could be used to indicate recent exposure of the fish to BaP/PAHs.     

孕期苯并(a)芘暴露对仔鼠肝细胞凋亡相关蛋白表达水平的影响

目的探讨孕期不同剂量苯并(a)芘暴露对仔鼠肝脏凋亡相关蛋白Bcl-xl和Bax表达水平的影响。方法将雌雄大鼠合笼后雌性SD大鼠见阴栓确定为受孕,以检出日为孕期第0 d。将孕鼠随机分为4组,每组8只,分为对照组(玉米油)和苯并(a)芘处理组(0.75 mg/kg、1.5 mg/kg和3 mg/kg)。从妊娠第3 d开始经灌胃苯并(a)芘直到妊娠第17 d结束,分别在孕0、4、7、14、19 d称孕鼠体重。待其自然分娩后24 h内测量仔鼠的体重、身长及尾长,然后取仔鼠肝脏,采用Western blot方法检测仔鼠肝脏中Bcl-xl和Bax蛋白的表达水平。结果随着孕期苯并(a)芘暴露水平的增加,新生仔鼠体重、身长、尾长等生长发育指标均有一定程度的下降,但未达到显著性差异(P>0.05)。Western blot结果显示,与对照组相比,中、高剂量染毒组仔鼠肝脏的Bcl-xl蛋白表达均明显下降,Bax蛋白表达均明显升高,差异均有统计学意义(P<0.05或P<0.01)。结论本研究建立了一种低水平的苯并(a)芘暴露模型,随着孕期苯并(a)芘染毒剂量的增加,新生仔鼠肝脏的凋亡相关蛋白Bcl-xl/Bax比值下降,提示细胞凋亡可能是参与孕期苯并(a)芘暴露导致新生仔鼠肝脏毒性作用的机制之一。     

Temporal changes of ethoxyresorufin-o-deethylase (EROD) activities and lysosome accumulation in intestine of fish on chronic exposure to dietary benzo[a]pyrene: linking erod induction to cytological effects

Temporal changes of intestinal and hepatic ethoxyresorufin-O-deethylase (EROD) activities and quantitative changes of secondary and tertiary (e.g., 2 degrees/3 degrees) lysosomes in enterocytes were compared for the juvenile grouper (Epinephelus coioides) on chronic exposure to foodborne benzo[a]pyrene (BaP) at two environmentally realistic levels (0.25 and 12.5 microg/g fish/d) over a four-week exposure and four-week depuration period. Intestinal EROD induction was rapid (within 3 d) and sustained in the BaP-exposed fish, while a fast recovery (within one week) was observed on withdrawal of BaP intake. A dose-response relationship was demonstrated between intestinal EROD activities and the levels of foodborne BaP. Conversely, hepatic EROD induction was weak and subsided rapidly in the exposed fish, signifying that hepatic EROD activity is not a good indicator of oral intake of BaP. Significant increase of 2 degrees/3 degrees lysosomes, as measured by Vv(lysosome, mucosa), was detected in young enterocytes of fish in the high-dosing group (12.5 microg/g fish/d) at exposure day 3 and persisted until recovery week 2. Importantly, intestinal EROD activity was significantly correlated to 2 degrees/3 degrees lysosome accumulation in enterocytes (r = 0.571, p < 0.001). These results further corroborate our earlier findings that induction of EROD activities in fish do not merely indicate exposure to BaP but also are correlated to harmful biological effects. We recommend the use of these two biochemical and cytological changes in intestines as specific biomarkers to indicate current and recent exposure of fish to BaP via oral intake.     

苯并[a]芘诱导内皮细胞细胞色素P4501A1表达的研究

目的：探讨苯并[a]芘(BaP)诱导猪主动脉内皮细胞细胞色素P4501A1(CYP1A1)表达及活性的影响。方法：离体培养猪主动脉内皮细胞，不同浓度BaP(0、0．5、1．0、5．0、10．0μmol／L)染毒24h，分别以Western-blot法和免疫组化方法检测不同浓度BaP诱导内皮细胞合成CYP1A1的影响，同时还探讨了乙氧基异吩噁唑-o-去乙氧基酶(EROD)活力的变化规律。结果：Western-blot法未能检测出对照组CYP1A1的表达，而各染毒组均检出了CYP1A1的表达；免疫组化结果显示染毒组仅在部分内皮细胞呈阳性反应；EROD活力诱导高峰的BaP浓度为0．5～1.0μmol／L。结论：BaP可诱导部分猪主动脉内皮细胞合成CYP1A1；EROD活力诱导高峰的BaP浓度为0．5～1．0μmol／L。     

Assessment of the bioavailability of PAHs in rats exposed to a polluted soil by natural routes: induction of EROD activity and DNA adducts and PAH burden in both liver and lung.

In order to assess bioavailability of polycyclic aromatic hydrocarbons (PAHs) present in soils, male laboratory rats were exposed to litters of control and polluted soils. After 88+/-2 h of exposure, several biomarkers were measured in both liver and lung. When rats were exposed to SIV soil, contaminated by a mixture of at least 13 PAHs, (1) only 2 or 3 PAH compounds were detected in liver and lung; (2) cytochrome P450-dependent monooxygenase activity, followed by 7-ethoxyresorufin O-deethylase (EROD) activity measurement, was highly induced in liver (13-fold-induction) and lung (up to 78-fold); and (3) DNA adducts were significantly increased. For what concerns soil artificially contaminated by only one PAH (phenanthrene or B[a]P), EROD activity was not or fully induced, respectively. These results demonstrate the occurrence of a high bioavailability of PAHs to mammals in natural conditions of exposure. First results concerning DNA adducts must be profound, but they already show that a short exposure of mammals to PAH-polluted soils can lead to potential genotoxic effects. EROD activity can be used as a sensitive biomarker in both liver and lung of rats maintained on litters of soils in the laboratory, and such a test can be used routinely to contribute to risk assessment.     

Anguilla anguilla L. biochemical and genotoxic responses to benzo[a]pyrene

Eels (Anguilla anguilla L.) were exposed for 2, 4, 6, 8, 16, 24, 48, 72, 144, and 216 h to 0 (control), 0.3, 0.9, and 2.7 microM benzo[a]pyrene (BaP). The biotransformation induced by BaP was measured as liver ethoxyresorufin O-deethylase (EROD) activity and cytochrome P450 content, and compared with the genotoxic effects, such as erythrocytic nuclear abnormalities (ENA), and blood and liver DNA strand breaks. The liver exhibited a highly significant EROD activity increase from 2 up to 216 h exposure to 0.9 and 2.7 microM BaP, whereas 0.3 microM BaP exposure induced a significant liver EROD increase from 2 up to 144 h. Liver cytochrome P-450 content was significantly increased at 8 h to 2.7 microM BaP exposure. Liver DNA integrity was decreased at 16 h, from 8 up to 144 h and 8 up to 72 h exposure to 0.3, 0.9, and 2.7 microM BaP, respectively. A significant decrease in blood DNA integrity was observed at 48, 72, 144 h, from 8 up to 72, and from 6 up to 72 h exposure to 0.3, 0.9, and 2.7 microM BaP, respectively. The A. anguilla L. genotoxic response to BaP, measured as ENA induction, was significantly increased at 144 h exposure to 0.3 microM BaP. The intermediate BaP concentration tested (0.9 microM) induced a significant three fold ENA increase at 48 and 72 h exposure compared to their controls. The highest BaP concentration (2.7 microM) induced a significant increase in ENA frequency at 72, 144 and 216 h exposure.     

Bioavailability of PCBs to Male Laboratory Rats Maintained on Litters of Contaminated Soils: PCB Burden and Induction of Alkoxyresorufin O-Dealkylase Activities in Liver and Lung

Male rats from the Sprague-Dawley laboratory strain were maintained in the laboratory during 3 days and 1 night on litters containing a reference soil and different amounts of a soil, mainly polluted by PCBs (207 ppm expressed in Aroclor? 1254; SIII soil). Two categories of biomarkers of exposure were measured in both liver and lung of these rats: PCB burdens and activities of microsomal liver and lung cytochrome P450–dependent mono-oxygenases, namely ethoxy-, pentoxy-, and benzoxy-resorufin O-dealkylase activities (EROD, PROD, and BROD, respectively). PCB burdens in liver and lung of rats exposed to SIII soil were 1,845 and 241 ppb, respectively (expressed in Aroclor? 1254 equivalents). EROD, PROD, and BROD were significantly induced in the liver of rats exposed to SIII soil, while only EROD activity was induced in the lung. Induction of hepatic EROD activity was ∼3- to 5.4-fold; pulmonary EROD activity was induced by 9- to 12-fold. In the lung, PROD and BROD activities were inhibited. When rats were exposed to SIII soil diluted with various amounts of standard ISO soil, a nearly linear dose-response relationship was found between the level of PCBs in the litter and EROD activity in both liver and lung. A nonlinear dose-response relationship exists with hepatic BROD activity; no dose-response relationship was observed with hepatic PROD and pulmonary PROD and BROD activities. EROD activity measurement in both liver and lung of rats maintained on a litter of PCB polluted soil was used to assess the bioavailability to mammals of PCBs. Received: 16 December 1996/Accepted: 18 November 1997     

Antioxidative effects of curcumin, β-myrcene and 1,8-cineole against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced oxidative stress in rats liver

The aim of this study was to investigate the effectiveness of curcumin, β-myrcene (myrcene) and 1,8-cineole (cineole) on antioxidant defense system in rats given a persistent environmental pollutant (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD). Rats (n = 112) were divided randomly into 8 equal groups. One group was kept as control and given corn oil as carrier. TCDD was orally administered at the dose of 2 μg/kg/week. Curcumin, myrcene and cineole were orally administered at the doses of 100 mg/kg/day, 200 mg/kg/day and 100 mg/kg/ day, respectively, by gavages dissolved in corn oil with and without TCDD. The liver samples were taken from half of all rats on day 30 and from the remaining half on day 60 for the determination of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), catalase (CAT), glutathione peroxidase (GSH-Px) and CuZn-SOD levels by spectrophotometric method. The results indicated that although TCDD significantly (p ≤ 0.01) increased formation of TBARS, it caused a significant decline in the levels of GSH, CAT, GSH-Px and CuZn-SOD in rats. In contrast, curcumin, myrcene and cineole significantly increased GSH, CAT, GSH-Px and CuZn-SOD levels but decreased formation of TBARS. Additionally, the antioxidative effects of curcumin, myrcene and cineole were increased at day 60 compared to day 30. In the TCDD groups given curcumin, myrcene and cineole, oxidative stress decreased by time. In conclusion, curcumin, myrcene and cineole showed antioxidant activity and eliminated TCDD-induced oxidative stress in rats in a time-dependent manner.     

Modulation of UDPglucuronosyltransferase activity in rats by dietary lipids

Male Wistar rats were fed for 40 d a purified diet whose lipid source (60 g/kg diet) was coconut, peanut, corn or fish (herring) oil. A low lipid (lipid-deficient) diet (corn oil, 2 g/kg diet) was also fed to some rats. There were no significant differences in final body weights of rats fed the coconut, peanut, and corn oil diets. Rats fed the fish oil diet gained less weight than those fed any other diet. However, liver weight, ratio of liver to body weight, and protein content were not affected by any of the diets. The plasma cholesterol concentration of rats fed fish oil was lower than that of the other groups of rats. This diet resulted in the highest cytochrome P-450 concentration and markedly enhanced epoxide hydrolase activity. No difference in the level in cytochrome P-450 was noted between the groups of rats fed the vegetable oils. Epoxide hydrolase activity was also significantly higher with the corn oil diet. Interestingly, only glucuronidation of group I substrates was stimulated by the fish or corn oil diets and lowered by the coconut oil diet. Liver microsomes of rats fed fish oil contained a high level of lipid peroxides; this diet greatly stimulated NADPH-dependent peroxidation. The differential stimulation of UDPglucuronosyltransferase activity towards group I substrates could be the results of a toxic action of the fish oil diet as suggested by the concomitant enhancements of epoxide hydrolase, transaminase activities and peroxide content.     

The Egyptian toad as a sensitive model to show the effect of corn oil on liver tumor induced by DMBA

The Egyptian toads, Bufo regularis, were divided into 5 groups, 100 each. Injections of 7,12-dimethylbenz(a)anthracene (DMBA) into the dorsal lymph sacs of toads induced liver tumors in 12% of the animals tested (12 toads out of 100 toads). The dose was 4mg/40g body weight administered once a week for 3 months. Toads treated with DMBA at the same dose level were subjected to commercial corn oil orally at dose levels 2cc/week, 2cc twice/week, 2cc 3 times/week. They showed higher incidence of liver tumors of 24%. 48% and 66% for the variable dose levels respectively. The minimum dose which increased tumor incidence was 2cc/week. It is concluded that the Egyptian toad can be used as a sensitive model for detecting the promoting effect of corn oil on liver tumors induced by DMBA.     

Dose- and time-dependent formation of biliary benzo[a]pyrene metabolites in the marine flatfish dab (Limanda limanda)

Polycyclic aromatic hydrocarbons (PAHs) are abundant pollutants, and many PAHs are carcinogenic, but only after metabolic activation. Benzo[a]pyrene (BaP) is among the most carcinogenic PAHs. The dose and time response of two enzymes involved in BaP metabolism and the amounts of BaP metabolites excreted into the bile were evaluated in an experiment with dab (Limanda limanda). Ninety dab were exposed orally to one of five doses of BaP (0, 0.08, 0.4, 2, or 10 mg/kg) and sampled at 3, 6, or 12 d after exposure. None of the doses studied caused significant induction of either microsomal ethoxyresorufin-O-deethylase (EROD). which reflects cytochrome P450 1A (CYP1A) activity, or cytosolic glutathione-S-transferase activity (GST). Concentrations of biliary BaP metabolites significantly increased with dose and significantly decreased with time after exposure. It is concluded that biliary BaP metabolites provide a much more sensitive method than EROD (CYP1A) or GST activity to monitor recent exposure to PAHs in dab.     

The effects of intramuscular and intraperitoneal injections of benzo[a]pyrene on selected biomarkers in Clarias gariepinus

This study investigated the dose-dependent and time-course effects of intramuscular (i.m.) and intraperitoneal (i.p.) injection of benzo[a]pyrene (BaP) on the biomarkers EROD activity, GST activity, concentrations of BaP metabolites in bile, and visceral fat deposits (Lipid Somatic Index, LSI) in African catfish (Clarias gariepinus). Intraperitoneal injection resulted in 4.5 times higher accumulation of total selected biliary FACs than i.m. injection. Hepatic GST activities were inhibited by BaP via both injection methods. Dose-response relationships between BaP injection and both biliary FAC concentrations and hepatic GST activities were linear in the i.p. injected group but nonlinear in the i.m. injected fish. Hepatic EROD activity and LSI were not significantly affected by BaP exposure by either injection route. We conclude that i.p. is a more effective route of exposure than i.m. for future ecotoxicological studies of PAH exposure in C. gariepinus.     

Gender-related differences in mouse hepatic ethanol metabolism

The effect of an acute oral load of 2 g ethanol/kg body weight was studied in a group of male and female 10-wk-old C3H/HeNCrj (C3H/He) mice to investigate gender change throughout differences of the hepatic ethanol metabolism of mice. The following parameters were measured in the serum from 0 h to 3 h after the start of the experiment: ethanol, acetaldehyde, and acetate. Their concentrations in the serum in female mice tended to show lower levels than in male mice. In female mice, the concentration of ethanol at 1 h and the concentration of acetate at 1 h, 2 h, and 3 h after ethanol administration showed significantly lower levels than in male mice. Ten-week-old male and female C3H/He mice were subcutaneously injected 50 microg/kg body weight beta-estradiol and 1.45 mmol/kg body weight testosterone propionate (testosterone) in olive oil, respectively, and changes in the activity of enzymes related to the hepatic ethanol metabolism of mice were examined at 24 h after the administration of sex hormones. The activity of the cytosolic alcohol dehydrogenase (ADH) and microsomal aniline hydroxylase (ANH) and the low Km, high Km and total aldehyde dehydrogenase (AlDH) activities in the mitochondrial, the cytosolic, and the microsomal fraction of the liver were higher. Moreover, the density of the band of CYP2E1 in the microsome in female mice was stronger than in male mice, and in the microsomal fraction of the liver, the total content of cytochrome P-450 (CYP) and ethoxyresorufin O-dealkylase (EROD) activity in male mice showed significantly higher values than in female mice. The density of the band of CYP2E1 and the three activities of AlDH in the hepatic mitochondrial fraction of male mice increased significantly under treatment with beta-estradiol. The three activities of AlDH of the cytosolic fraction of the liver in female mice significantly decreased under treatment with testosterone. The present findings suggested that in C3H/He mice livers, the rate of ethanol metabolism is faster in females than in males, and the enzymes related to ethanol metabolism are controlled by testosterone or beta-estradiol. It is suggested that ethanol and its metabolite disappear faster from the serum of female mice than from the serum of male mice because the activities of hepatic enzymes related to ethanol metabolism are higher in female mice than in male mice. C3H/He mice, hepatic ethanol metabolism, gender different, ADH, AlDH     

Dietary Canola Oil Suppressed Growth of Implanted MDA-MB 231 Human Breast Tumors in Nude Mice

Long chain omega 3 (n-3) fatty acids, eicosapentaenoic (EPA) and/or docosahexaenoic acid (DHA), have been shown to suppress growth of most cancer cells. In vivo, alpha linolenic acid (ALA, 18:3n-3) can be converted to EPA or DHA. We hypothesized that substituting canola oil (10% ALA) for the corn oil (1% ALA) in the diet of cancer bearing mice would slow tumor growth by increasing n-3 fatty acids in the diet. Sixty nude mice received MDA-MB 231 human breast cancer cells and were fed a diet containing 8% w/w corn oil until the mean tumor volume was 60 mm ³ . The dietary fat of half of the tumor bearing mice was then changed to 8% w/w canola oil. Compared to mice that consumed the corn oil containing diet, the mice that consumed the canola oil containing diet had significantly more EPA and DHA in both tumors and livers, and the mean tumor growth rate and cell proliferation in the tumor were significantly slower (P < 0.05). About 25 days after diet change, mice that consumed the corn oil diet stopped gaining weight, whereas the mice that consumed the canola oil diet continued normal weight gain. Use of canola oil instead of corn oil in the diet may be a reasonable means to increase consumption of n-3 fatty acids with potential significance for slowing growth of residual cancer cells in cancer survivors.     

Identification of carcinogens in cooking oil fumes.

According to earlier studies, fumes from cooking oils were found to be genotoxic in several short-term tests such as the Ames test, sister chromatid exchange, and SOS chromotest. Fume samples from six different commercial cooking oils (safflower, olive, coconut, mustard, vegetable, and corn) frequently used in Taiwan were collected. Polycyclic aromatic hydrocarbons (PAHs) were extracted from the air samples and identified by high-performance liquid chromatography and confirmed by gas chromatography/mass spectrometry. Extracts of fumes from safflower oil, vegetable oil, and corn oil contained benzo[a]pyrene (BaP), dibenz[a,h]anthracene (DBahA), benzo[b]fluoranthene (BbFA), and benzo[a]anthracene (BaA). Concentrations of BaP, DbahA, BbFA, and BaA were 2.1, 2.8, 1.8, and 2.5 microg/m3 in fumes from safflower oil; 2.7, 3.2, 2.6, and 2.1 microg/m3 in vegetable oil; and 2.6, 2.4, 2.0, and 1.9 microg/m3 in corn oil, respectively. The authors constructed models to study the efficacy of table-edged fume extractors used commonly by Taiwanese restaurants. Concentrations of BaP were significantly decreased when the fume extractor was working (P<0.05) and the average reduction in percentage was 75%. The other identified PAHs were undetected. These results indicated that exposure to cooking oil fumes could possibly increase exposure to PAHs, which may be linked to an increased risk of lung cancer. The potential carcinogenic exposure could be reduced by placing table-edged fume extractors near cooking pots.     

松仁油对高脂小鼠体重、血脂水平以及脂质过氧化的影响

目的探讨松仁油对喂食高脂饲料小鼠体重、血脂水平及脂质过氧化的影响。方法分别以高脂饲料(20%猪油和80%基础饲料,HF)及高脂饲料加松仁油(20%松仁油和80%高脂饲料,SHF)饲喂小鼠。于45d和90d测体脂含量及血脂水平,并取脑和肝脏制成匀浆液测丙二醛(MDA)、脂褐质(LP)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性。结果松仁油可影响小鼠体重并使高脂小鼠血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)含量降低,而高密度脂蛋白胆固醇(HDL-C)升高,提示松仁油具有调节血脂的作用。与正常组比,高脂小鼠脑和肝组织的CAT、总SOD和GSH-Px活性均显著降低,MDA和LP含量显著升高,提示高脂饲料可促进小鼠脑和肝组织脂质过氧化。松仁油组与高脂组比,小鼠脑和肝组织的CAT、总SOD和GSH-PX活性显著升高,MDA含量显著降低,提示松仁油可降低因高脂饲料引起的小鼠脂质过氧化。     

Combustion-related organic species in temporally resolved urban airborne particulate matter

Accurate characterization of the chemical composition of particulate matter (PM) is essential for improved understanding of source attribution and resultant health impacts. To explore this, we conducted ambient monitoring of a suite of 15 combustion-related organic species in temporally resolved PM_2.5 samples during an ongoing animal exposure study in a near source environment in Detroit, MI. All of the 15 species detected were above the method detection limit in 8 h samples. This study focused on two molecular classes: polycyclic aromatic hydrocarbons (PAHs) and hopanes measured in samples. Of the 12 PAHs studied, benzo[b]fluoranthene (169 pg m^?3), benzo[g,h,i]perylene (124 pg m^?3), and benzo[e]pyrene (118 pg m^?3) exhibited the three highest mean concentrations while 17α(H),21β(H)-hopane (189 pg m^?3) and 17α(H),21β(H)-30-norhopane (145 pg m^?3) had the highest mean concentrations of the three hopanes analyzed in samples. Ratios of individual compound concentrations to total compound concentrations (∑15 compounds) showed the greatest daily variation for 17α(H),21β(H)-hopane (11–28%) and 17α(H),21β(H)-30-norhopane (8–20%). Diagnostic PAH concentration ratios ([IP]/[IP + BP] (range 0.30–0.45), [BaP]/[BaP + BeP] (range 0.26–0.44), [BaP]/[BP] (range 0.41–0.82), [Bb]/[Bk] (range 2.07–2.66)) in samples reflected impacts from a mixture of combustion sources consistent with greater prevalence of petroleum combustion source emissions (gasoline, diesel, kerosene, and crude oil) compared to coal or wood combustion emissions impacts at this urban site. Results from this study demonstrate that short-duration sampling for organic speciation provides temporally relevant exposure information.     

延胡索酸二甲酯对大鼠醌还原酶和谷胱甘肽—S—转移酶的诱导作用

目的　探讨延胡索酸二甲酯（ＤＭＦ） 对大鼠主要脏器醌还原酶和谷胱甘肽Ｓ转移酶的诱导作用和意义。方法　雄性Ｗｉｓｔａｒ 大鼠饮食中补充０ ．２ ％ ＤＭＦ,于６ 、２４ 、７２ 小时、１ 和２ 周后取血并处死动物,用酶动力学法测定大鼠腺胃、肝、肺、肾和心脏中的醌还原酶（ＱＲ） 和谷胱甘肽Ｓ转移酶（ＧＳＴｓ） 活性,并按此法测定血清ＱＲ、ＧＰＴ和乳酸脱氢酶含量。结果　服用ＤＭＦ２４ 、７２ 小时、１ 和２ 周后可观察到腺胃、肝、肺、肾脏中ＱＲ 和ＧＳＴｓ 活性显著增高（ Ｐ＜ ０ ．０００ １ 或Ｐ＜ ０ ．０１） ,同时血清ＱＲ 活性也显著增高（ Ｐ＜ ０ ．０１ ,或Ｐ＜ ０ ．０００ １） 。ＤＭＦ对血清ＧＰＴ 和乳酸脱氢酶的活性则无影响。结论　ＤＭＦ对大鼠腺胃、肝、肺、肾和血清中的ＱＲ 和ＧＳＴｓ 活性具有诱导作用,ＤＭＦ有望成为人类抗氧化损伤的保护剂和解毒剂。     

Differential effect of high dietary iron on α-tocopherol and retinol levels in the liver and serum of mice fed olive oil– and corn oil–enriched diets

The influence of dietary fats on cellular α-tocopherol and retinol uptake in iron overload is poorly understood. The aim of this study was to investigate the effect of a high-iron diet on the retinol and α-tocopherol levels in mice fed olive oil– and corn oil–enriched diets. Mice were fed for 3 weeks a standard mouse chow (the control group) and diets enriched with 5% by weight of corn oil or olive oil. Diets of the mice fed corn oil and olive oil were additionally supplemented with 1% by weight carbonyl iron. Both dietary oils and iron increased the liver iron uptake. High-iron feeding induced oxidative stress in mice liver, measured as a thiobarbituric acid-reactive substance level. Both fats and iron induced changes in the liver fatty acid composition. Liver retinol and α-tocopherol stores increased with iron supplementation in the olive oil–enriched diet, with a simultaneous decrease in serum. The results suggest that the influx of α-tocopherol and retinol from serum to the liver is induced by high dietary iron. This redistribution appears to be stronger for retinol than for α-tocopherol and is also higher in mice fed olive oil than in mice fed corn oil, suggesting that the composition of dietary lipids is important in the treatment of high-iron tissue conditions. In conclusion, the results of this study suggest that the increase of hepatic α-tocopherol and retinol levels in the olive oil–based diet is a dietary-dependent responsive mechanism that probably is not primarily related to an increased risk of oxidative damage induced by high-iron intake.