米非司酮对早孕小鼠促性腺激素细胞的形态学影响

研究米非司酮终止早孕时小鼠垂体促性腺激素细胞——FSH细胞、LH细胞的形态学变化。方法:应用免疫组织化学PAP方法,对FSH细胞与LH细胞的阳性细胞密度,细胞质内激素颗粒进行观察。结果:实验组与对照组比较,FSH细胞的阳性细胞密度,细胞质内FSH颗粒无显著性差异;LH细胞的阳性细胞密度,细胞质内LH颗粒均明显减少,有显著性差异(P<0.05)。结论:米非司酮对早孕小鼠的FSH细胞的功能无明显影响;对LH细胞的功能有显著的抑制作用。     

Effect of late follicular phase administration of antide on ovulation and inhibin secretion in macaques

In previous studies, the LHRH antagonist detirelix, administered to stumptailed macaques during the menstrual cycle, was only partially effective in blocking pituitary-ovarian function when given during the late follicular phase. Since the antagonist was suppressive when administered during the early luteal phase, we investigated the ability of antide, a putative long-acting LHRH antagonist, to cause inhibition of the LH surge or luteal function when administered during the late follicular phase. Six animals with regular ovulatory cycles were treated on day 10 of the follicular phase with 1mg/kg antide s.c. All animals demonstrated a continued rise in serum concentrations of estradiol which were followed by an LH surge beginning 2–5 days after antide injection and serum progesterone and inhibin secretion which indicated normal luteal function. In a second experiment, six animals were treated on day 10 of the follicular phase with 3mg/kg antide s.c. In three animals, this caused a fall in serum concentrations of estradiol and the expected LH surge and rises in progesterone and inhibin secretion indicating ovulation failed to occur. In 2 animals,the LH surge was not prevented but the consequential rise in progesterone and inhibin was attenuated. In the remaining animal the cycle appeared unaffected. Pharmacokinetics of antide revealed an initial high release rate during the first 4 days (1mg/kg) or 6 days (3mg/kg) followed by a period of sustained release at a relatively low level. These results show that antide is partially effective in blocking ovulation at a high dose in the macaque and may result in an inadequate luteal phase, presumably as a result of its extended action.     

二硫化碳对雌性大鼠性腺毒性机制的初步研究

目的 探讨CS2对下丘脑－垂体－卵巢轴平衡调节功能的影响机制。方法 对SD大鼠给予不同剂量CS2（每天400mg/kg、100mg/kg)染毒不同时间（14d、28d)后,测定大鼠动情期血清中激素FSH、LH、P、E2含量变化及动情间期给予GnRH刺激试验。结果 随着染毒剂量的增大或染毒时间的延长,大鼠均不同程度地出现动情周期延长,甚至出现动情期消失,CS2染毒大鼠卵巢重／比重比值与对照组比较,显著增高且具有显著差异（P＜0．05）。各染毒组（每天400mg/kg、110mg/kg染毒14d物100mg/kg染毒28d)与对照组比较,血清LH水平显著增高,且有显著性差异（P＜0．05）。除高剂量组大鼠在注射GnRH60min后血清P的含量显著高于对照组及低剂量组,且均有显著性差异（P＜0．05）,外,各剂量组的大鼠血清的各激素水平均未显著性差异（P＞0．05）。结论 在本实验条件下,CS2对雌性性腺功能具有损害作用,GnRH刺激试验结果提示垂体储备功能尚未降低,但不能排除是由于大鼠对GnRH的超度反应所致。     

Lead poisoning and reproduction: effects on pituitary and serum gonadotropins in neonatal rats.

In order to investigate the effects of neonatal lead poisoning on pituitary gonadotropic function, newborn rats were given daily doses of lead (25, 100, and 200 mg/kg) by gastric gavage. Control rats were given deionized water. Groups of animals were sacrificed at 10, 15, and 20 days of age and serum and pituitary levels of the gonadotropins follicle stimulating hormone (FSH) as well as pituitary contents of luteninizing hormone (LH) were determined by radioimmunoassay. Lead concentrations in blood, bone, brain, and pituitary tissues of similarly treated 15-day-old rats were determined by atomic absorption spectrometry. Lead content in bone (femur) and brain showed dose-dependent elevations throughout the dose range; in blood, it reached a plateau of about 1000 μg% already at the dose of 100 mg/kg/day. Lead remained at undetectable levels (<0.01 μg/g) in pituitary tissue regardless of the dose. There were no significant differences between lead-treated and control rats in body weights, pituitary weights, pituitary LH contents in either sex, and serum FSH levels in males. Lead exposure increased pituitary FSH content in male rats at all ages studied, and suppressed serum FSH levels in 15-day-old females. These results suggest that the effects of subclinical neonatal lead poisoning on gonadal development and subsequent function, especially in the female, may be mediated by central neuroendocrine mechanisms.     

Effect of levonorgestrel-releasing intrauterine device on hormonal profile and menstrual pattern after long-term use

In the present study 14 women after 6 years' use of levonorgestrel-releasing IUD were investigated for the changes of LH, progesterone (P), estradiol (E₂), prolactin (PRL) and serum binding globulin (SHBG) in relation to the levonorgestrel levels throughout a segment of 26–40 days with the aim of comparing the hormonal profiles with those during the first year of use of Lng-IUD. Ultrasound scanning was used to follow the development of follicles along with the RIA measurement of hormones. The results of serum LH, P and E₂ showed ovulation in 11 cases with either normal menstrual cycles (5 cases), prolonged or irregular cycles (4 cases) or with amenorrhea for 2–3 years (2 cases). One case showed insufficiency of luteal function and 2 cases showed anovulation but with follicular hyperactivity. Higher percentages of ovulatory cycles (78.5%) were found after 6 years of use. No case of complete suppression of ovulation was found. Anovulatory cycles only constituted 14.3%. Clinically, the development of follicles followed by ultrasound scanning further confirmed the hormonal findings. The persistent enlargement of follicles coincided with high levels of E₂. After 6 years of use, the serum levels of levonorgestrel were still maintained at mean levels of 314.26 pmol/L and 470.63 pmol/L in the ovulatory and anovulatory groups, respectively. It is concluded that over two-thirds of the cases have ovulatory cycles after long-term use of Lng-IUD; the contraceptive effect is mainly due to its local action on the endometrium, with much less effect on the ovarian function.     

正己烷对雌性大鼠性腺毒性作用实验研究

[目的]探讨正己烷的雌性性腺毒性及其机制。[方法]对雌性Wistar大鼠给予3种剂量正己烷（162mg／kg、566mg／kg和1980mg／kg）腹腔注射染毒,1次／d,每周5d,持续7周观察大鼠动情周期变化。测定大鼠动情期血清中激素FSH、LH、E2和P含量,观察子宫、卵巢脏器系数以及子宫内膜腔上皮厚度。[结果]随着染毒剂量的增大,大鼠均不同程度地出现动情期的延长。与对照组相比。卵巢脏器系数升高。各剂量组子宫内膜腔上皮厚度与对照组相比降低。各剂量组大鼠血清FSH、LH、E2和P水平与对照组类似。[结论]正己烷能引起明显的雌性性腺毒性,卵巢是其毒作用的萤要靶器官之一。     

4-氯-2-氟-3-甲氧基苯硼酸的急性毒性研究

目的探讨4-氯-2-氟-3-甲氧基苯硼酸的急性经口毒性,急性经皮毒性,急性皮肤刺激和急性眼刺激性.方法 按照《化学品测试方法》(国家环境保护总局,2004年)开展急性经口毒性试验,急性经皮毒性试验,急性皮肤刺激试验和急性眼刺激性试验. 结果①急性经口毒性试验:雌性大鼠急性经口LD₅₀为369mg/kg,95%可信区间为227mg/kg~599mg/kg;雄性大鼠急性经口LD₅₀为233mg/kg,95%可信区间为160mg/kg ~399mg/kg.对死亡大鼠解剖见肺脏充血.②急性经皮毒性试验:大鼠急性经皮LD₅₀ >2500mg/kg.③急性皮肤刺激试验:对大耳白兔染毒后各观察时点皮肤刺激反应总积分平均值和皮肤刺激反应时点最高积分均值均为0分.④急性眼刺激性试验:对大耳白兔眼刺激试验分级为5级.结论 4-氯-2-氟-3-甲氧基苯硼酸对雌雄性大鼠急性经口毒性分别属"低毒","中毒".靶器官可能是肺脏;对大鼠急性经皮毒性属"实际无毒";对大耳白兔皮肤不产生刺激性,但可对眼睛产生中等刺激性.     

Estradiol reduces cumulative mercury and associated disturbances in the hypothalamus-pituitary axis of ovariectomized rats

The aim of this research was to verify the incidence of endocrine dysfunction associated with mercury intoxication in the hypothalamus-pituitary reproductive system of normally cycling or castrated female rats and the possible protective action of estrogen replacement therapy. We found no differences in the frequency of estrus cycle stages (diestrus I, diestrus II, proestrus, and estrus) in normally cycling female rats during 54 days of daily oral administration of 0.004, 0.02, and 1 mg/kg MeHgCl. Conversely, the higher dose (1 mg/kg) induced a significant decrease in content of luteinizing hormone releasing hormone (LHRH) into the medial hypothalamus when administered daily during 3 days in ovariectomized rats. This effect was associated with increased levels of mercury found in the anterior pituitary gland and medial hypothalamus, rather than the anterior and posterior hypothalamus, striatum or cerebellum. A decrease in plasma levels of luteinizing hormone (LH) was also detected after administration of 7.5 mg/kg MeHgCl. These disturbances in LHRH and LH secretion induced by mercury were abolished or superimposed (respectively) by estrogenic replacement therapy (0.025 mg/kg 17beta estradiol cypionate, intramuscular). These effects were associated with a significant reduction in mercury content of the anterior pituitary gland and medial hypothalamus, suggesting a protective estrogenic effect.     

亚砷酸钠致脏器细胞DNA链断裂的实验研究

目的 观察不同剂量亚砷酸钠(NaAsO₂)在不同时相引发小鼠体内细胞DNA链断裂损伤的影响.方法 采用单细胞凝胶电泳法(SCGE)分别测定ICR小鼠皮下注射NaAsO₂0.4,2,10mg/kg后1,3,6h的脾脏、胸腺、骨髓和肝细胞的DNA链断裂损伤.结果 不同剂量亚砷酸钠注射后,可以发现2和10mg/kgNaAsO₂可诱发脾细胞、胸腺细胞、骨髓细胞DNA链断裂,各组出现的彗星细胞百分比明显高于对照组,同时DNA迁移距离也较对照组明显增大;而在染毒后不同时相观察的结果表明,NaAsO₂诱发脾细胞出现DNA链断裂损伤在1h最为明显,而胸腺细胞和骨髓细胞相对较晚,DNA链断裂损伤高峰出现在染毒3h;染毒6h,各种组织细胞的DNA链断裂损伤开始减少,逐渐趋于正常.各剂量组及时间点均未观察到亚砷酸钠有诱导肝细胞DNA链断裂损伤的作用.结论 2mg/kg和10mg/kgNaAsO₂可诱发小鼠体内脾、胸腺和骨髓细胞的DNA链断裂损伤,但不同细胞对NaAsO₂作用的反应性不完全一致.     

Anovulatory luteal cycles in primates

The short-term therapy with gonadotropins and inhibitors of prostaglandin synthesis was administered to 12 adult cycling cynomolgus monkeys to study morphology and functions of anovulatory luteinized follicles. In Group 1, five monkeys (6 cycles) received human menopausal gonadotropin (hMG 10 I.U. FSH/10 I.U. LH per 1 kg) on cycle day (c.d.) 5 and 6. Human chorionic gonadotropin (hCG 50 I.U. per 1 kg) and hMG (5 I.U. LH and 5 I.U. FSH per 1 kg) were given at 12:00 on c.d. 7. Indomethacin (15 mg/kg) was injected at 16:30 on c.d. 7 and 08:30 on c.d. 8. Ovarian biopsy was obtained in 2 cycles. In Group 2, 7 monkeys (33 cycles) received single injection of hCG (50 I.U./kg) and hMG (5 I.U. FSH/5 I.U. LH/kg) four to one days before the expected ovulation. Two doses of Naproxen-sodium were given orally 4 and 20 hours later. After treatment, females were kept with males for 5 to 7 days. Laparotomy was performed one week after treatment. Ovarian biopsy was obtained in 5 cycles. Treatment in the midfollicular phase caused premature luteinization of the follicles and suppression of ovulation in all cycles. Histological studies revealed presence of luteinized follicles. Serum progesterone was elevated. Luteal phase averaged 13.6 days (vs. 15.8 days in ovulatory cycles). Treatment in the late follicular phase resulted in luteinization of the dominant follicle and inhibition of ovulation in 20 (61%) cycles. Luteal phase lasted 17.1 days. Serum progesterone was elevated to low or midluteal values. Gross evidence of ovulation was present in 13 (39%) cycles. One pregnancy occurred. All monkeys returned to regular, ovulatory cycles after the experiments were terminated.     

镍铬钴混合物对肾毒作用机理的研究

目的 探讨镍铬钴混合物致肾毒作用机理,为早期防治镍、铬、钴联合毒性所致的肾脏损伤提供理论依据。方法 模拟金川矿区矿石中镍、铬、钴平均含量百分比(Ni:Cr:Co=0.26:0.30:0.02),连续10日小鼠腹腔注射硫酸镍2.5mg/kg、重铬酸钾0.14mg/kg、氯化钴0.41mg/kg及其混合物0.09mg/kg、0.17mg/kg染毒。制备肾小管细胞膜,采用定磷比色法检测肾小管细胞膜Na⁺.K⁺-ATPase、Ca²⁺-ATPase活性。结果 各单体和混合物明显抑制肾小管细胞膜Na⁺.K⁺-ATPase、Ca²⁺-ATPase活性,尤以混合物组显着,并且混合物毒性大于各单体毒作用。结论 混合物在体内可能产生联合毒性,抑制肾小管细胞膜ATPase活性而致肾脏损伤。     

邻苯二甲酸二乙基已酯对未成年小鼠卵巢发育影响

目的观察邻苯二甲酸二乙基己酯(DEHP)对卵泡生长发育和性激素分泌影响,探讨DEHP对未成年雌性小鼠卵巢发育的毒性作用。方法将60只未成年(3周龄)清洁级ICR雌性小鼠随机分为4组,分别为对照(玉米油)组和低、中、高剂量 DEHP染毒组(100、400、1 600 mg/kg),每组15只,采用灌胃方式染毒,染毒容量为0.1 mL/kg,每天1次,每周5 d,连续6周;染毒结束后,检测小鼠血清促卵泡生成激素(FSH)、促黄体生成激素(LH)、雌激素、孕激素水平,取出小鼠卵巢组织连续切片观察卵巢各级卵泡数目构成比。结果 高剂量DEHP组血清中FSH水平为(0.72±0.04) mIU/mL 高于对照组的 (0.58±0.30) mIU/mL,差异有统计学意义(P<0.05);与对照组[(1.74±0.17) pg/mL]比较,低、中剂量DEHP组小鼠血清中雌激素水平[(1.62±0.18)、(1.69±0.16) pg/mL]均降低,高剂量组[(2.11±0.04) pg/mL]升高,差异均有统计学意义(P<0.05);各剂量染毒组LH和孕激素水平与对照组比较差异均无统计学意义。结论 DEHP暴露对未成年雌性小鼠的卵巢发育具有毒性作用。     

The pyrethroid pesticide esfenvalerate suppresses the afternoon rise of luteinizing hormone and delays puberty in female rats

BACKGROUND: One of the most widely used classes of insecticides is the synthetic pyrethroids. Although pyrethroids are less acutely toxic to humans than to insects, in vitro studies have suggested that pyrethroids may be estrogenic. OBJECTIVES: We assessed pubertal effects by orally administering 0.5, 1.0, and 5.0 mg/kg/day of the type II pyrethroid esfenvalerate (ESF) to female rats beginning on postnatal day (PND) 22 until vaginal opening. ESF administration suppresses serum estradiol and delays pubertal onset. MATERIALS AND METHODS: To assess possible hypothalamic and/or pituitary effects, animals received 0.5 or 1.0 mg/kg ESF or corn oil on PNDs 22-29. On PND30, we drew three blood samples (200 microL) from each rat at 15-min intervals beginning at 1000 hours, and again at 1500 hours. To test hypothalamic responsiveness, after the third afternoon sample, all animals received an intravenous injection of N-methyl-d,l-aspartic acid (NMA; 40 mg/kg), and then we drew two more samples. We performed a second experiment as above except that animals received luteinizing hormone-releasing hormone (LHRH; 25 ng/rat) to test pituitary responsiveness. RESULTS: Basal levels of luteinizing hormone (LH) in the afternoon hours were higher in control animals than in animals treated with 1.0 mg/kg ESF (p < 0.05). Furthermore, NMA- and LHRH-stimulated LH release was similar in control and ESF-treated animals, indicating that both hypothalamic and pituitary responsiveness, respectively, were unaffected. CONCLUSIONS: Although the hypothalamus is able to respond to exogenous stimuli, absence of a normal afternoon rise in LH would indicate a hypothalamic deficit in ESF-treated animals.     

Inhibitory effects of treatment with an LHRH antagonist on the ovulatory cycle are reduced when administered during the late follicular phase

To compare the effects of transitory suppression of pituitary gonadotropin secretion by an LHRH antagonist at the mid or late follicular phase of the menstrual cycle, adult macaques with normal menstrual cycles were treated with an LHRH antagonist (N-Ac-D-Nal(2)1,D-pCl-Phe2,D-Trp3,D-hArg(Et2)6,D-Ala10 ]LHRH (detirelix) administered subcutaneously at a dose of 300 micrograms/kg, daily for 3 days beginning either during the mid or late follicular phase. In all eight animals treated during the mid follicular phase, serum concentrations of LH and FSH declined and remained suppressed for 4 days. This caused a fall in serum concentrations of estradiol and the expected ovulation failed to occur. During the recovery period a marked rise in serum FSH occurred followed by normal follicular development and ovulation 14.8 +/- 0.6 days after the last injection of antagonist. Of the 9 macaques given the same treatment during the late follicular phase, only in two was the expected rise in serum progesterone prevented. In 4 of the animals a transitory suppression in LH and estradiol was observed but this was followed by a recovery and occurrence of an LH surge and rise in serum progesterone indicating ovulation during the course of treatment. In the remaining 3 macaques treatment commenced on the day of the initiation of the LH surge and was associated with a progesterone rise of normal duration but lower than normal magnitude during the early luteal phase. These results show that LHRH antagonist treatment causes rapid inhibition of pituitary-ovarian function when administered up to the mid follicular phase of the cycle and is effective in blocking ovulation. The suppressive effects of the antagonist are reduced when administered during the late follicular phase. This may be due to decreased dependence of the pituitary gonadotrope on LHRH at this time and on decreased dependence of the dominant follicle on the gonadotropins.     

Ovulation inhibition by estetrol in an in vivo model

BACKGROUND: Currently, the synthetic steroid ethinylestradiol (EE) is the preferred estrogen in combined oral contraceptives. The aim of the present study was to evaluate the effectiveness of the natural steroid estetrol (E(4)) as an ovulation inhibitor in rats when compared to EE. STUDY DESIGN: Regularly cycling female rats were treated orally twice daily for four consecutive days, starting on the day of estrus, with E(4) (0.03, 0.1, 0.3, 1.0 or 3.0 mg/kg), EE (0.0003, 0.001, 0.003, 0.01 or 0.03 mg/kg) or vehicle control (eight animals per group). In a second experiment conducted under the same experimental protocol, 2.0 mg/kg of E(4) was administered as a single daily dose or as a dose of 1.0 mg/kg twice daily. In both studies, the primary end point was the number of ovulated oocytes in the genital tract. RESULTS: Estetrol at the twice daily dose of 0.3 mg/kg and above inhibited ovulation. This effect was statistically significant (p<.05). The comparator, EE, significantly inhibited ovulation (p<.05) at the highest dose (0.03 mg/kg) administered twice daily. An E4 dose of 2.0 mg/kg administered once daily for four consecutive days inhibited ovulation in four of eight rats. In contrast, when the same dose was administered in two separate doses, that is, 1.0 mg/kg twice daily, ovulation was inhibited in eight of eight rats. The ED(50) for the EE and the E(4) dose response curves shows that EE is 18 times more potent than E(4). CONCLUSION: Twice daily administration of E(4) effectively inhibits ovulation in cycling rats. The effect is dose-dependent. The relative potency of E(4) is about 18 times less compared to that of EE. We conclude that based on these data, combined with available pharmacological and clinical data on the safety and efficacy of E(4), the human fetal estrogenic steroid estetrol is a potential candidate to replace EE in combined oral contraceptives.     

The effect of combined oral contraceptive steroids on the gonadotropin responses to LH-RH in lactating women with regular menstrual cycles resumed

The effect of combined oral contraceptive steroids upon pituitary response to stimulation with 100 μg LH-RH was studied in both non-puerperal and lactating women with regular menstrual cycles. Serum prolactin concentration was 14.20 ng/ml in non-puerperal women whereas it was 39.37 ng/ml in lactating women. A comparability was shown in the LH response to LH-RH in non-puerperal women and lactating women. FSH response to LH-RH, however, was significantly exaggerated in lactating-menstruating women as compared to that of non-puerperal women.

Combined oral contraceptive steroids lowered basal levels of LH and FSH in non-puerperal women and lactating women although the difference was not statistically significant in non-puerperal women. The LH and FSH maximal responses to LH-RH were significantly diminished in both non-puerperal and lactating women on combined oral contraceptives. There was, however, no difference in the mean LH or FSH responses between non-puerperal women and lactating women.

Combined oral contraceptive steroids used in this study seemed to suppress ovulation by decreasing the pituitary responsiveness to LH-RH in lactating-menstruating women as well as in normally menstruating women.     

亮丙瑞林在体外受精-胚胎移植长方案促排卵中的降调节效果观察

目的:观察国产亮丙瑞林在体外受精-胚胎移植(IVF-ET)治疗中长方案超促排卵的降调节效果。方法:回顾性分析2010年4月～2011年5月在青岛大学医学院附属医院生殖医学中心接受IVF-ET/ICSI治疗应用长方案控制性超促排卵148例患者的临床资料。其中32例采用国产亮丙瑞林(亮丙瑞林组)1.2 mg于黄体中期皮下注射进行垂体降调,116例采用达菲林(达菲林组)1.2 mg于黄体中期肌肉注射进行垂体降调。分析比较两组的降调节效果和IVF-ET的结局。结果:两组均达垂体降调标准,月经第2天血清E2、FSH、LH水平比较差异均无统计学意义(均P>0.05);两组获卵数、受精率、优质胚胎数、种植率、临床妊娠率比较差异均无统计学意义(均P>0.05)。结论:在IVF-ET长方案超促排卵中,国产亮丙瑞林1.2 mg黄体中期皮下注射可达到控制性超促排卵的垂体降调节作用,与达菲林具有相同的临床治疗效果。     

Pituitary, ovarian and endometrial effects of graded doses of medroxyprogesterone acetate administered on cycle days 7 to 10

Eighteen apparently healthy women with normal menstrual cycles were studied during a control cycle and then during a treatment cycle, in which graded doses (2.5, 5.0 and 10 mg/day) of medroxyprogesterone acetate (MPA) were administered orally on cycle days 7 to 10. In both the control and the treatment cycle peripheral blood was drawn daily for the assay of luteinizing hormone (LH), estradiol (E₂) and progesterone (PROG) and an endometrial biopsy was taken on cycle day 11.

The lowest dose of MPA (2.5 mg × 4) did not influence the various cycle characteristics. Administration of higher doses (5.0 or 10 mg × 4) resulted in a lengthening of the duration of E₂ -peak (P < 0.05), an increase in the area under the E₂ -peak (P < 0.05), a decrease in the area under the PROG-curve (P < 0.05) and a reduction in the height of the LH-peak (P < 0.05). Furthermore, in 5 of these 12 subjects there was no ovulatory-like PROG-pattern during the cycle in which MPA was administered for 4 days.     

复合营养素对PM_(2.5)所致大鼠急性肺部氧化应激和炎症损伤的影响

目的探讨某复合营养素对大气PM_(2.5)致大鼠急性肺部氧化应激和炎症损伤的预防作用。方法将40只SD大鼠随机分为4组:空白组、PM_(2.5)模型组、低剂量营养素(150 mg/kg)+PM_(2.5)组、高剂量营养素(750 mg/kg)+PM_(2.5)组。营养素组连续预灌胃14 d营养素溶液,空白组、模型组灌胃生理盐水。第15天灌胃后除空白组外的各组大鼠气管滴注PM_(2.5)(9.0 mg/kg)混悬液染毒,每隔24 h 1次,共3次,空白组气管滴注生理盐水。末次染毒24 h后,收集血样、支气管肺泡灌洗液、肺组织匀浆和病理切片。分析测定血清丙二醛(MDA)、超氧化物歧化酶(SOD)水平,肺泡灌洗液中乳酸脱氢酶(LDH)、酸性磷酸酶(ACP)水平;肺匀浆液中肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)水平。结果与空白组比较,PM_(2.5)模型组的大鼠MDA、ACP、LDH、TNF-α、IL-1β水平增加、SOD活力降低(P<0.05或P<0.01);与PM_(2.5)模型组比较,高、低剂量营养素+PM_(2.5)组能降低MDA、TNF-α、IL-1β水平及升高SOD活力(P<0.05或P<0.01),高剂量营养素+PM_(2.5)组能降低ACP、LDH水平(P<0.05或P<0.01),并改善大鼠肺组织病理变化。结论该复合营养素对PM_(2.5)致大鼠急性肺部氧化应激及炎症损伤具有保护作用。     

磷酸钠对砷致细胞膜损伤保护作用

目的 探讨磷酸钠对三价砷所致细胞膜损伤的保护作用。方法 用NaAsO₂处理非洲绿猴肾上皮细胞(Vero)后,在培养液中加入不同剂量磷酸钠剂,采用分光光度法分别测定细胞膜Na⁺,K⁺-ATP酶活性,高效液相法测定细胞膜磷脂组分含量改变。结果 2.20mg/L剂量的砷暴露可明显抑制Vero细胞膜Na⁺,K⁺-ATP酶活性;高剂量磷酸钠(69.00 mg/L)干预后,Na⁺,K⁺-ATP酶活性为(0.761±0.067)U/(mgprot.h)高于砷染毒组(0.544±0.037)U/(mgprot.h)(P<0.05);69.00 mg/L磷酸钠组细胞膜磷脂酰胆碱、磷脂酰乙醇胺、磷脂酰丝氨酸及神经鞘磷脂含量分别为(0.506±0.073),(0.101±0.237),(0.083±0.005)和(0.066±0.003)mg/mL,明显高于砷染毒组(P<0.05)。结论 一定剂量磷酸钠对砷染毒细胞的细胞膜Na⁺,K⁺-ATP酶活性及磷脂组分的改变具有保护作用。