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PubMed1981

Male-female differences in the cytotoxic activity of human monocytes in vitro.

The cytotoxic activity of human monocytes towards anti-D-sensitized Rh(D)-positive red cells in vitro was studied in relation to the age and sex of healthy monocyte donors. It was found that cytotoxic activity of monocytes from young females (age range 18-40 years) was significantly less than that of monocytes from age-matched males, irrespective of the use of oral contraceptives. No such difference was found between monocytes from older males and females (age range 43-63 years). The cytotoxic activity of monocytes from the two latter groups of donors was similar to that of young males. In the presence of cytochalasin B, which enhances the cytotoxic activity of monocytes, no male-female difference was detected, indicating that the maximal cytotoxic capacity of monocytes from young females is similar to that of monocytes from young males. We have previously presented evidence that the cytotoxic activity of monocytes is mediated by lysosomal enzymes released by these cells. These present data suggest that the reduction in cytotoxic activity of monocytes from young females might be a result of a reduced lysosomal enzyme release which is possibly related to the in vivo action of female sex hormones. However, we were not able to detect an inhibitory effect of oestrogens and progestagens on cytotoxic activity of monocytes from males in vitro.

Adolescent↗
PubMed1975

Immunological measurement of transferrin compared with chemical measurement of total iron-binding capacity.

Because of uncertainty as to the molecular weight of transferrin, a previous comparison [Von der Heul et al., Clin. Chim. Acta 38, 347 (1972)] between transferrin content of serum and total iron-binding capacity cannot be definitive. We found a conversion factor for expressing the maximum amount of iron bound by 1 mg of transferrin. We compared the resulting calculated value with values obtained by three other methods for measuring total iron-binding capacity. We agree with the previous observation that the latter, as measured radioisotopically, give higher results than would be judged from the transferrin content but the same as those for two chemical methods. The diffusion rate of transferrin in agar was the same irrespective of the degree of iron saturation. Serum transferrin concentrations were low in patients with anemia resulting from malignancy, chronic disorders, and cirrhosis of the liver, and high or normal in patients with iron deficiency anemia and in pregnant women or women who were taking birth-control pills. Measurement of transferrin concentration can be used to distinguish iron deficiency anemia from anemia resulting from chronic disorders, but offers no advantages over existing methods for estimating total iron-binding capacity.

Anemia↗
PubMed2000

[Clinic-epidemiological significance of drug hepatotoxicity in liver disease consultation].

To assess epidemiological and clinical significance of drug hepatotoxicity in the setting of liver diseases consultation, ten thousand and three hundred forty two prospectively designed clinical records from patient cared for in our Liver Unit in the period 1988-1998 were incorporated into the study; 58 out of 10,342 (prevalence = 5.6%) fulfilled at least the first three of the following causality requirements: 1.--Liver injury associated in time to drug exposition; 2.--Negative evaluation of more common other etiologies; (alcohol, viruses, immunologic, metabolic, etc) 3.--Favourable response to drug withdrawal (ALT < 50% of baseline in 8 to 30 days in acute hepatitis type, and alkaline phosphatase and/or total bilirubin < 50% of baseline up to 6 months, in acute cholestasis) 4.--Inadverted or rarely prescribed positive challenge. Acute hepatitis type of injury were considered when serum ALT rise 8 times or more above normal superior level with alkaline phosphatase (APh) below 3 times; "pure" cholestasis when APh rise 3 times or more above normal with ALT below 8 times; mixed acute injury or cholestatic hepatitis when both ALT and APh were elevated above 8 and 3 times respectively, and indeterminate type when both enzymes were below the referred levels. Chronic injury were considered when six or more month of evolution and compatible liver histology happens. Clinical severity were expressed as mild (absence of major clinical complications, serum bilirubin < 5 mg/dl and prothrombin concentration > 75%), moderate (presence of clinical complications, bilirubin > 5 mg/dl and prothrombin concentration between 50-75%), and severe (major clinical complications with bilirubin > 5 mg/dl and prothrombin concentration < 50%). Female/male ratio was 1.4:1, with age average 39 years (R = 15-77) and major concentration of cases above 40. More than 50% of cases received 2 or more drugs. Jaundice was present in 60.4%, and systemic manifestations of hypersensibility (fever, adenomegalies, rush, mononucleosis like syndrome, eosinophilia) in 29.3%. Acute injury represented 91.4% of the cases: 41.4% acute hepatitis, 15.5% "pure" cholestasis, 24.1% cholestatic hepatitis, and 10.3% indeterminate type. Four patients (4.5% of acute injury cases) were presented as severe acute liver failure, leading to liver transplant in one of them, drug association (INH-rifampicin and carbamazepine-phenobarbital) and inadverted challenge (sulphonamides and pemoline) were associated to clinical severity. Chronic injury were found in five patient (8.6%), four of them associated to chronic hepatitis and the other one to a ductopenic syndrome. Six drugs represented 53.4% of our cases; oral contraceptives (7 cases), INH alone or combined with rifampicin (6 cases), sulfonamides and clorpropamida (5 cases each), carbamazepine and amiodarone (4 cases each). Normalization of liver enzymes after drug suppression took 2 to 8 weeks in acute hepatitis type (X = 4 weeks), 4 to 20 in "pure" cholestasis (X = 12 weeks) and 8 to 24 weeks in cholestatic hepatitis or mixed type (X = 16 weeks). Two cases of chronic hepatitis normalize the histological activity index in 20 and 18 month respectively, one case remains as chronic hepatitis at 10 month and the other one progress to cirrhosis; the ductopenic syndrome normalize histology in 19 months receiving urso-deoxicolic acid, 10 mg/k/day.

Acute Disease↗
PubMed1993

Adverse effects of drugs and chemicals in breast milk on the nursing infant.

Breastfeeding is an essential physiologic process that provides nutrition to the infant and protects the child against infection and immunologic disorders. The incidence of various diseases and metabolic disorders is known to be less in a breastfed infant compared with a child given a milk substitute. Psychologically, a breastfed infant forms a maternal bond that enables adaptation more readily to a social environment. It is well-established that all drugs are excreted into breast milk and are bioavailable to the infant. In general the majority of drugs do not pose a significant problem to the nursing infant and breastfeeding should be encouraged. The physician should be aware of which drugs are contraindicated during lactation and which drugs should be used with caution. There are also environmental chemicals that readily enter breast milk and may induce adverse effects. At present, the advantages of breastfeeding for infant development outweigh the potential adverse consequences and this physiologic process should be encouraged. With the use of available data on pharmacokinetics, milk-to-plasma ratio, excretion, etc. a supportive approach can be delineated by the pediatrician to reassure the nursing mother that they can safely breastfeed and continue therapy with minimal effects on the infant. It is thus imperative to document the extent to which a drug or chemical appears in breast milk and any apparent effects in the infant.

Alcohol Drinking↗
PubMed1987

Search for circulating immune complexes and activation of the complement system in relation to estrogen treatment.

By employing an ammonium sulphate precipitation technique, previous studies have shown circulating immune complexes (cIC) in an increased proportion of women using oral contraceptives, as compared with non-users. The pathogenicity of cIC is well established, as deposition in organs may lead to activation of the complement system and thereby inflammation and tissue destruction. The purpose of the present study was to determine whether estrogen treatment could induce the formation of cIC, as measured by more specific immune complex assays. To test for complement activation, plasma samples were analysed for the complement split product C3d. Thirty-one women treated with estrogen for menopausal hormone deficiency symptoms and 38 untreated controls were analysed for cIC. Using a solid-phase C1q-anti-IgG binding assay, the mean level of cIC in the estrogen-treated group did not differ significantly from that of the untreated control group (p greater than 0.05). In a solid-phase C1q-protein A binding assay a very small average increase in the cIC values for the estrogen-treated group in comparison with the untreated group was found, expressing a significant difference (p = 0.04). Moreover, the C3d levels for the estrogen-treated group did not differ from the untreated control group. Finally, no differences could be demonstrated in cIC and C3d levels between patients treated with synthetic estrogens and patients treated with natural estrogens.

Antigen-Antibody Complex↗
PubMed1983

[Mode of action of intrauterine devices].

The intrauterine foreign bodies (IUFB) used in a series of the authors' experiments were made of stainless steel, plastics, copper wire, and silicone rubber. The experiments were done as follows: Firstly, the implantive influence of IUFB was examined. It was found (1) that the embryo might be implanted above or below the position of the foreign body but not at the position of the foreign body and (2) that the existing 5 different kinds of foreign bodies possessed the same antifertility effect. Secondly, the washing fluid of uterine cavities with foreign bodies was examined for studying biochemical component, immunologic reaction in respect of blood coagulating factors and white cell counts and its differential counts. The results of these experiments did not give any significant statistical meaning except in so far as the protein nitrogen and white cell counts were concerned. The authors have investigated the results of the contrast group by statistical methods, which showed no significant change, but it was found that the polymorphonuclear leukocyte counts are proportional to the amount of protein nitrogen contained. In the experiments, the authors did not observe any relationship existing between the uterine foreign bodies and the increase of macrophages. Thirdly, the morphology of the endometrium in contact with intrauterine foreign bodies was examined by light, scanning, and transmission electron microscopy. The results of these observations showed that the phenomenon of the endometrium can be divided into 3 conditions: (1) the accumulated mucus formed a thin or thick layer like a screen covering the surface of the endometrium; (2) the erosions and ulcers appeared on the surface of the endometrium with some white cell infiltration; and (3) sometimes, necrosis of the endometrium and bleeding ensued, 1 or another of these phenomena might happen in all the samples but one. The authors, therefore, conclude that the antifertility effect of an interauterine foreign body must prevent the embryo from implantation. This effect may be caused by the pressure and stimulation of the foreign bodies, which induce unspecialized reaction with moderate exudation and necrosis in the tissue.

Biology↗
PubMed1988

Oxidation of 17 alpha-ethynylestradiol by human liver cytochrome P-450.

One of the classic examples of adverse drug interactions involves pregnancies in women using the oral contraceptive 17 alpha-ethynylestradiol who also ingest rifampicin or barbiturates or hydantoins. Previous work had demonstrated increased metabolism (2-hydroxylation) of 17 alpha-ethynylestradiol in individuals using rifampicin. In this report evidence is presented for the involvement of a specific form of human cytochrome P-450, termed P-450NF, in this phenomenon. Although purified P-450NF has only relatively low catalytic 17 alpha-ethynylestradiol 2-hydroxylase activity, antibodies raised to P-450NF specifically inhibited greater than 90% of the activity in liver microsomes which had either high or low catalytic activity. When different liver samples were compared, rates of microsomal 17 alpha-ethynylestradiol 2-hydroxylation were highly correlated with amounts of immunochemically measured P-450NF or rates of nifedipine oxidation, a characteristic activity of P-450NF. Prior incubation of human liver microsomes with NADPH and troleandomycin resulted in decreased 17 alpha-ethynylestradiol 2-hydroxylation. In addition, 17 alpha-ethynylestradiol appears to be a mechanism-based inhibitor in human liver microsomes, as shown by the loss of both spectrally detectable cytochrome P-450 and 17 alpha-ethynylestradiol 2-hydroxylase activity during incubation in the presence of NADPH. Additional experiments did not show any evidence for the involvement of a number of other human cytochrome P-450 enzymes in 17 alpha-ethynylestradiol 2-hydroxylation (i.e., P-450DB, P-450PA, P-450MP, P-450j). These results are consistent with the view that P-450NF is the major enzyme involved in 17 alpha-ethynylestradiol oxidation and that drugs and hormones which influence the expression and activity of this enzyme can influence the efficacy and side effects of this compound.

Cytochrome P-450 Enzyme Inhibitors↗
PubMed2003

[C3d molecular adjuvant increases the immunity of human chorionic gonadotropin beta DNA contraceptive vaccination and changes its immune response from Th1 to Th2].

OBJECTIVE: To testify the effect of C3d molecular adjuvant on the immunogenicity of human chorionic gonadotropin beta (hCG beta) DNA vaccination as well as the mode of immune response. METHODS: BALB/c mice aged 6 weeks were immunized intramuscularly two times at an interval of 3 weeks with by the plasmid pcDNA3 (A1-3 groups), pcDNA3-hCG beta (B-3 groups), pcDNA3-hCG beta-C3d3 (C1-3 groups), or pCMV4-hCG beta-C3d3 (D1-3 groups), at dosage of 5 pmol, 10 pmol, and 20 pmol, respectively. Three weeks after the second vaccination the animals were killed, specimens of their peripheral blood were extracted to determine the anti-hCG beta antibody titer by indirect ELISA. Their spleen cells were harvested and stimulated in vitro by hCG antigen for 24 hours. The Th1/Th2 cytokines in the culture supernatant were determined by ELISA. RESULTS: At the dosage of 20 pmol, C3d molecular adjuvant significantly enhanced the anti-hCG beta antibody titer. The utmost anti-hCG beta antibody titer of C3 group was 1:450, 9 times higher than that of B3 group, and the utmost anti-hCG beta antibody titer of D3 group was 1:12 150, 243 times higher than that of B3 group. Stimulated in vitro by 5,000 IU hCG beta antigen, the splenic cells of the C3 and D3 immunization group produced significantly lower IL-2, INF-gamma and TNF-alpha than those of the B3 immunization group (P < 0.01 or P < 0.05). The IL-4 level of the C3 group was higher than that of the B3 group while the IL-10 level of the D3 group was significantly higher than that of the B3 group (P < 0.01). CONCLUSIONS: The C3d molecular adjuvant increases significantly the hCG beta immunogenicity of hCG beta DNA vaccination; meanwhile decreases the secretion of Th1 cytokines (IL-2, INF-gamma, and TNF-alpha), and increases the expression of Th2 cytokines (IL-4 and IL-10) in response to hCG antigen. So C3d changes the anti-hCG immune response from Th1 type to Th2 type.

Adjuvants, Immunologic↗
PubMed2000

Mediation of the immunomodulatory effect of beta-estradiol on inflammatory responses by inhibition of recruitment and activation of inflammatory cells and their gene expression of TNF-alpha and IFN-gamma.

BACKGROUND: Estrogen has long been reported to show immunomodulatory effects on immune responses, yet, its specific anti-inflammatory mechanism is not clear. METHODS: In this study, we analyzed the effects of beta-estradiol (E2), at its contraceptive dose, on both T cell-independent and T cell-dependent inflammations, and the associated immune mechanism, in female mice. The T cell-independent inflammation was locally induced either with an intradermal injection of olive oil in the footpad, or by an intraperitoneal injection of proteose peptone (PP). The T cell-dependent inflammation was induced by an intraperitoneal injection of the purified protein derivatives (PPD). RESULTS: While E2 inhibited olive oil-induced inflammation as monitored by the decrease in footpad swelling, it did not affect the gene expression of monocyte chemoattractant protein-1 and IL-6 by cells at the inflammatory locus. E2 also inhibited PP-induced inflammation as monitored by the decrease in the number of inflammatory peritoneal exudate cells (PEC) coinciding with a marked decrease in the number of macrophages and granulocytes (Gr. 1+). While E2 did not affect the gene expression of monocyte chemoattractant protein-1 and IL-6 by PP-elicited PEC, it decreased both gene expression and production of TNF-alpha. E2 also decreased the number of cells expressing the lymphocyte function-activated protein-1 in PP-elicited PEC, but not for CD62L. In purified protein derivative-induced T cell-dependent inflammation, E2 decreased the total cellularity of PEC and the relative numbers of CD3+ and CD4+ T cells, and the number of cells expressing the lymphocyte activation markers CD40, CD44, CD69 and IL-2Ralpha in PEC. Furthermore, while E2 did not affect the gene expression of the early T lymphocyte activation protein-1 by PEC, it decreased the gene expression of INF-gamma. CONCLUSION: Collectively, the results suggest that E2-mediated inhibition of inflammatory responses may be due to a combination of suppression of homing and activation of inflammatory cells and their production of TNF-alpha and IFN-gamma.

Adjuvants, Immunologic↗