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At least 19 recordsLinked to original sources
PubMed1990

Serosurvey of prevalence of human immunodeficiency virus amongst high risk groups in Port Sudan, Sudan.

During October, 1987, 593 sera were collected from risk groups in Sudan's only major deepwater port, Port Sudan. The risk groups included prostitutes, lorry drivers and prisoners. A large proportion of the study participants practised high risk behaviour which included sexual promiscuity, medical treatment by injection, scarification and tattooing. Despite high risk behaviour and evidence of a high prevalence of hepatitis B infection, a virus transmitted in a manner similar to HIV, no study participants were positive for HIV infection. This data suggests that the prevalence of HIV infection amongst high risk groups in Port Sudan is very low. These findings confirm a lack of clinical cases of AIDS in hospitalized patients in Port Sudan and the small number of reported cases in other areas of northern Sudan.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Evaluation of febrile patients in Port Sudan, Sudan: isolation of dengue virus.

One hundred consecutive patients admitted to the Port Sudan Hospital with a temperature greater than or equal to 100 degrees F were evaluated. Enteric fever was diagnosed in 19 patients and malaria in 13. Virologic studies identified 21 cases of dengue infection. One dengue 1 and 17 dengue 2 infections were diagnosed by viral isolation. Three untyped dengue infections were identified serologically. The clinical presentation and course of patients infected with dengue virus were most consistent with classic dengue fever. There was no evidence of hemorrhagic phenomena or shock in any of the dengue-infected patients. Both dengue 1 and 2 must be considered causes of acute fever in East Africa.

Adolescent↗
PubMed1984

Utilization of primary health services in Port Sudan, Sudan.

The utilization of primary health services provided by two health centres and a hospital out-patient department was studied. The epidemiologic pattern was similar in the three health care facilities; minor gastrointestinal tract, respiratory tract and skin conditions formed the majority of cases. Distance was a limiting factor for utilization of health services in the health centres and not in the hospital. The average consultation time per patient was two minutes. Lack of drugs was the universal problem. Suggestions and recommendations to solve some of the problems and improve services are presented.

Adolescent↗
PubMed1990

Mechanism of formation and 32P-postlabeling of DNA adducts derived from peroxidative activation of carcinogenic non-aminoazo dye 1-phenylazo-2-hydroxynaphthalene (Sudan I).

Horseradish peroxidase in the presence of hydrogen peroxide mediates the activation of carcinogenic 1-phenylazo-2-hydroxynaphthalene (Sudan I) to DNA-bound products in vitro. The peroxidase activating system is greater than 10 times more effective with respect to DNA modification by Sudan I than the microsomal enzymes containing cytochrome P450. The DNA-binding reaction of the Sudan I metabolite(s) formed by the peroxidase system is dependent on Sudan I and H2O2 concentration and pH. Reactive intermediate(s) or product(s) of the Sudan I oxidation by peroxidase with a short half-life are responsible for the DNA modification. DNA modified by peroxidase-activated Sudan I becomes colored and has an absorption maximum at approximately 480 nm. The modification of DNA by Sudan I metabolites(s) formed by the peroxidase system is inhibited by some compounds of physiological importance (ascorbate, glutathione, Mg2+ ions) and by radical trapping agents (nitrosobenzene, methyl viologen). 32P-Postlabeling assay of the DNA modified by Sudan I activated by the peroxidase system indicates that the covalent DNA adduct formation is the principal type of the DNA modification. Four major and several minor adducts of deoxyribonucleotide 3',5'-bisphosphate from DNA with Sudan I metabolite(s) were detected by the classical Randerath 32P-postlabelling assay as well as by the nuclease P1 version of the same method.

Animals↗
PubMed1991

Identification of contact allergens in C.I. Solvent Red 23 (commercial Sudan III) by chemical analysis and animal testing.

C.I. Solvent Red 23, commercial Sudan III, is widely used in cosmetic products. Chemical analyses and guinea pig sensitization tests were carried out to identify its contact allergens. In the Magnusson & Kligman guinea pig maximization test, C.I. Solvent Red 23 showed 20% positive reactions. By conducting chemical analyses with HPLC and GLC, 2-naphthol (82 ppm), azobenzene (48 ppm), Sudan I (570 ppm) and many unknown impurities, as well as the main constituent pigment Sudan III (87%), were found. The chemical structure of one unknown impurity was identified as an isomer of Sudan III. We found that purified Sudan III showed no positive reaction, while the isomer elicited 30% positive reactions, in the same guinea pig test. Furthermore, cross-sensitization with p-phenylenediamine was investigated using the guinea pig test. Animals sensitized with p-phenylenediamine also showed positive elicitation reactions with purified Sudan III. From these results, the contact allergenicity of C.I. Solvent Red 23 is considered to be due to impurities, including the isomer of Sudan III, 1-(o-phenylazophenylazo)-2-naphthol. Positive reactions to Sudan III previously demonstrated in hairdressers are due to cross-sensitivity with p-phenylenediamine.

Allergens↗
PubMed1983

Biological effects of the Sudan dyes. Role of the Ah cytosolic receptor.

The hepatic induction of two cytochrome P1-450-mediated activities [aryl hydrocarbon hydroxylase (AHH) and ethoxyresorufin O-deethylase (ETR)] was studied following the administration of the azo dyes Sudan I, II, III, and IV. When using Ah-responsive C57BL/6J mice, Sudan dye II proved to be quite potent as an inducer causing almost maximal induction at doses as low as 40 mg/kg (1.4 mumoles/kg body weight); Sudan dyes I, III and IV caused one-half the maximal induction at four times that dose. In contrast, none of these compounds caused induction of AHH or ETR in the Ah-nonresponsive DBA/2J animals. When the dyes were given to B6D2F1 X D2 backcross progeny, a strict correlation with the presence of the Ahb allele and the inducibility of AHH and ETR was observed. When these compounds were examined as agonists for the Ah cytosolic receptor by their capacity to replace [3H]2,3,7,8-tetrachlorodibenzo-p-dioxin binding, Sudan dye II was substantially more effective than Sudan dyes I, III and IV. When four repeated doses of Sudan dye II were administered intraperitoneally to Ah-responsive C57BL/6J mice and Ah-nonresponsive DBA/2J mice, Sudan dye II-induced immunotoxicity was markedly greater in C57BL/6J compared to DBA/2J mice.

Animals↗
PubMed1984

The effect of Sudan III on drug metabolizing enzymes.

We have examined the induction of drug metabolizing enzymes in rat liver microsomes by azo dye, 1-(p-phenylazophenylazo)-2-naphthol (Sudan III). Marked increases were observed in the levels of cytochrome P-448 as well as in p-nitroanisole O-demethylase (p-NAD), amaranth (AR) and neoprontosil reductases (NPR) and 7-ethoxycoumarin O-deethylase (ECD) activities. On the other hand, aminopyrene N-demethylase activity was not significantly increased. Further, induced ECD activity was inhibited 90% by a specific antibody against cytochrome P-448 while the inhibition observed with an antibody against cytochrome P-450 was less than 25%. Simultaneous administration of Sudan III and 3-methylcholanthene (3-MC) induced cytochrome P-448 up to a level brought about by either Sudan III or 3-MC treatment alone. In contrast, Sudan III did not induce cytochrome P-448 in the 3-MC insensitive DBA/2 mouse. Solubilized microsomes from Sudan III-treated rats showed an identical sodium dodecyl sulfate polyacrylamide gel electrophoretic (SDS-PAGE) pattern with those from 3-MC-treated animals. It is concluded that the cytochrome P-448 induced in liver by Sudan III is very similar to that induced by 3-MC. Sudan III also induced UDP-glucuronyltransferase activity towards 1-naphthol and estradiol. It did not induce NADPH-cytochrome c reductase, nor any of the enzymes which constitute the microsomal electron transport chain except for cytochrome P-448.

Animals↗
PubMed1988

Role of specific cytochrome P-450 isoenzymes in the regio-selective metabolism of 7,12-dimethylbenz[a]anthracene in microsomes from rats treated with phenobarbital or Sudan III.

The rates of formation of diols of dimethylbenz[a]anthracene (DMBA-3,4-diol, DMBA-5,6-diol and DMBA-8,9-diol) have been determined in hepatic microsomes prepared from untreated rats or from animals treated with phenobarbital (PB) or Sudan III. PB treatment enhanced the formation of the proximate carcinogen, DMBA-3,4-diol, and of the 5,6-diol while treatment with Sudan III suppressed the formation of DMBA-3,4-diol but greatly increased the rates of formation of the other two diols. Metyrapone, a reagent which is specific for members of the major PB-induced cytochrome P-450 subfamily (P-450-PB3), did not alter the rate of formation of the diols other than in microsomes prepared from PB-treated animals in which formation of the 5,6-diol was inhibited. Incubation of DMBA with microsomes resulted in the formation of covalent, DMBA-microsome adducts. Treatment of the animals with PB and Sudan III increased the rate of formation of DMBA-microsome adducts to a similar extent (approximately 5-fold). The formation of adducts could be inhibited by metyrapone in microsomes from untreated and PB-treated animals but the reagent had no effect on adduct formation in microsomes from Sudan III-treated animals. These observations may indicate that adduct formation in microsomes from Sudan-treated animals involves primary epoxide metabolites while in microsomes from PB-treated animals secondary metabolites are involved and these may be formed by a P-450-PB3 isoenzyme. Specific P-450 isoenzymes involved in the regioselective formation of DMBA-diols have been identified by the use of antibodies directed against specific isoenzymes. An antibody to P-450-MC1b inhibited the formation of DMBA-5,6-diol and 8,9-diol in microsomes from Sudan III-treated animals. Western blot analysis demonstrated that P-450-MC1b was induced in microsomes of animals treated with Sudan III but was not present in the other two microsomal preparations. In accord with the observations with metyrapone, anti-P-450-PB3 inhibited formation of DMBA-5,6-diol in microsomes from PB-treated animals but was without effect on the formation of other diols. Anti-P450-PB1 inhibited the formation of DMBA-3,4-diol in microsomes from PB-treated animals. Western blot analysis of microsomes from animals treated with several xenobiotics indicated a qualitative correlation between the content of P-450-PB1 and the rate at which DMBA-3,4-diol was formed.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Suppression of 7,12-dimethylbenz[a]anthracene-induced chromosome aberrations in rat bone marrow cells after treatment with Sudan III and related azo dyes.

Noninbred Long-Evans rats fed Sudan III at 24 hours before they were given an injection of 7,12-dimethylbenz[a]anthracene (DMBA) displayed prominently suppressed DMBA-induced chromosome aberrations (CA) in their bone marrow cells. Rats fed Sudan III simultaneously with the DMBA injection showed no suppressed CA effect. The suppressive effect of Sudan III on DMBA-induced CA paralleled the dose rate of Sudan III when given in the range between 1 and 10 mg Sudan III/kg body weight; higher doses produced no additional suppression. The capacity of various Sudan III-related chemicals to prevent DMBA-induced CA paralleled their capacity to prevent DMBA-induced adrenal apoplexy and mammary cancer. Among the azo dyes investigated, Sudan III was most efficient in protecting against DMBA-induced CA. Polychlorinated biphenyl and phenobarbital, inducers of drug-metabolizing enzymes, also suppressed DMBA-induced CA.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1989

HIV-1 and hepatitis B transmission in Sudan.

A seroepidemiologic survey was conducted among 773 male soldiers living in five urban locations in Sudan to study the prevalence of and risk factors for HIV-1 and hepatitis B transmission. Twenty-eight per cent of the study population were born and raised in southern Sudan, an area bordering Kenya, Zaire and Uganda, whilst 72% of the study subjects were from northern Sudan. Seventy-eight per cent of the study population had serologic evidence of past hepatitis B infection, and 13 soldiers were confirmed positive for HIV-1 antibody. All 13 HIV-positive soldiers had recently been deployed in southern Sudan. Multivariate analysis indicated an association between living in southern Sudan and both hepatitis B (odds ratio 8.2) and HIV-1 infection (odds ratio 14). Additionally, sexual relations with prostitutes (odds ratio 1.5) and medical injections for schistosomiasis (odds ratio 2.72) were independent predictors of hepatitis B markers in this military population. The findings of this study suggest that sexual promiscuity is a risk factor for hepatitis B transmission in Sudan. They also indicate one possible route for the spread of HIV-1 from central to northern Africa.

Acquired Immunodeficiency Syndrome↗
PubMed1981

Allergy to castor bean in the Sudan: measurement of serum IgE and specific IgE antibodies.

Allergy to castor bean was diagnosed in thirty-nine dockworkers from Port Sudan, on the basis of rhinitis and/or asthma provoked by castor bean dust, together with a positive prick test to a high dilution of castor bean extract. These were compared to twelve non-allergic dockworkers from Port Sudan and forty-three other Port Sudan residents. The castor bean allergic group had significantly higher IgE levels (mean 902 iu/ml) than the non-allergic dock workers (mean 245 iu/ml) or the Port Sudan residents (mean 404 iu/ml) P less than 0.01. IgE antibody to castor bean was detected in all the castor bean-allergic group, and also in 25-35% of the Port Sudan resident group, but at a much lower level. No evidence was found to support the view that parasitic infestation (evidenced by IgE antibodies to Ascaris lumbricoides) prevented sensitization to castor bean or any other allergen. There was a higher incidence of IgE antibodies to Dermatophagoides pteronyssinus in the castor bean-allergic dockworkers (18/36) than in the non-allergic Port Sudan residents (5/43), although we were unable to show that sensitivity to other inhalant allergens pre-disposed to castor bean allergy.

Allergens↗
PubMed1981

Urolithiasis in the Sudan. Studies on a stone-prone and a stone-free population.

Biochemical studies were performed on 80 adult males with renal stones and 24 controls from Northern Sudan. Similar studies were performed on 44 controls from Southern Sudan, where urinary stones rarely occur. No significant differences between stone formers and controls from Northern Sudan were found regarding serum uric acid, phosphate, alkaline phosphatase, total protein, albumen, daily urine calcium or uric acid. Similarly, no significant difference was found between 2 groups in the incidence of hypercalciuria, hyperuricaemia of hyperuricosuria. The serum calcium was significantly higher in stone formers. The mean serum and daily urine calcium were significantly lower, and the mean serum and daily urine uric acid were significantly higher in controls from Southern Sudan compared to either stone formers or controls from Northern Sudan. The mean daily urine volume was significantly higher in Southern controls compared to Northern controls. The increased prevalence of stone formers in Northern Sudan appears to result from the higher calcium output in the urine and the lower urine volume in the North compared with the South.

Adult↗
PubMed1990

Characterization of epidemic and nonepidemic Neisseria meningitidis serogroup A strains from Sudan and Sweden.

A random selection of 25 strains isolated during an epidemic caused by serogroup A Neisseria meningitidis in Sudan (1988), 3 preepidemic meningococcal strains (1985), and 26 serogroup A strains isolated from sporadic cases of meningitis in Sweden (1973 to 1987) were assessed for multilocus enzyme genotypes (ETs), DNA restriction enzyme patterns, outer membrane proteins, lipopolysaccharides, pilus formation, and antibiograms. All of the 25 Sudanese epidemic isolates and 22 of the Swedish strains were of the same or closely related ETs (ETs 3, 4, and 5), corresponding to clone III-1, which has been responsible for two pandemic waves in the last three decades. The earlier pandemic involved Scandinavia, and the last one caused an outbreak during the pilgrimage to Mecca, Saudi Arabia (August 1987), spreading to Sudan, Chad, and Ethiopia. The three Sudanese preepidemic isolates (1985) were clone IV-1 (sulfonamide susceptible), which has been resident in the African meningitis belt for the last 25 years. The uniformity of clone III-1 strains (all sulfonamide resistant) from Sudan and Sweden was confirmed by DNA restriction enzyme patterns. ETs 3, 4, and 5 from Sudan and Sweden had 86 to 100% similarity to a Swedish clone III-1 reference strain, whereas ETs 1, 2, 6, and 7 showed 50 to 80% similarity. Class 1 protein for clone III-1 showed serosubtype antigens P1.9 and P1.x, whereas ET6 strains (clone IV-1) had serosubtype P1.7. Lipopolysaccharides were variable in the Sudanese and Swedish strains. Pili were expressed in all clone III-1 isolates from Sudan and Sweden but in none of the clone IV-1 isolates (Sudan, 1985).

Antigenic Variation↗
PubMed1990

Childhood acute bacterial meningitis in the Sudan: an epidemiological, clinical and laboratory study.

The aims of the present study were to document the epidemiology, clinical features and complications of childhood acute bacterial meningitis (ABM) in The Sudan during both an inter-epidemic (endemic) period (1985-1986), and the 1988 serogroup A epidemic; and to examine the phenotypic and genetic similarities and differences of Neisseria meningitidis strains isolated in The Sudan and Sweden. A new enzyme immunoassay test (Pharmacia Meningitis EIA-Test) was evaluated as a potential rapid diagnostic method for the detection of Haemophilus influenzae (HI) type b, Neisseria meningitidis (MC) and Streptococcus pneumoniae (PNC). The test was found to have good sensitivity (0.86) and specificity (0.95) in the inter-epidemic period; and to be adaptable to the field work in The Sudan during the 1988 MC epidemic. During inter-epidemic (endemic) situations in The Sudan, greater than 90% of childhood ABM was caused by one of the three organisms, HI type b, MC and PNC. HI accounted for 57% of the cases. The peak incidence (76%) of HI cases was in infants (less than 12 months) similar to the situation in other African countries. The overall case fatality ratio was 18.6%. Prospective follow-up of survivors for 3-4 years revealed that an additional 43% either died or had permanent neurological complications, the most prevalent and persistent of which was sensorineural hearing loss recorded in 22% of long term survivors. Post-meningitic children were found to have significantly lower intelligence quotients (92.3 +/- 13.9) than their sibling controls (100.7 +/- 10.2, P = 0.029). Features of the large serogroup A sulphonamide resistant MC epidemic (February-August 1988) in Khartoum are described. An estimated annual incidence of 1,679/100,000 was recorded at the peak of the epidemic. The highest attack rate was in young children less than 5 years, as in many other African countries; nevertheless, a high morbidity was observed in adults (31% of the cases greater than or equal to 20 years). The clinical features, mortality (6.3%) and short term sequelae in Sudanese children were generally within the framework described for MC disease elsewhere. Detailed analysis of MC isolates from Sudan and Sweden by characterizing their electrophoretic enzyme types, DNA restriction endonuclease pattern and outer membrane proteins, revealed that serogroup A MC clone III-1 was responsible of The Sudan epidemic in 1988 and has been the dominant serogroup A organism in Sweden since 1973. The Sudanese strains isolated prior to the epidemic (1985) were clone IV-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1995

Paradoxical effect of Sudan III on the in vivo and in vitro genotoxicity elicited by 7,12-dimethylbenz(a)anthracene.

Effect of the induction of drug metabolizing enzymes by Sudan III on the in vivo and in vitro genotoxicity elicited by 7,12-dimethyl-benz(a)anthracene (DMBA) was investigated. A significant suppression of DMBA-induced micronucleated reticulocytes was observed in C57BL/6 mice treated with Sudan III intraperitoneally for 3 or 5 days before injection of the DMBA. However, the preincubation of DMBA with hepatic microsomes from Sudan III-treated rats caused a marked increase in the in vitro mutagenicity in the Ames assay, paradoxically. Sudan III was found to induce CYP 1A1, 7-ethoxycoumarin O-deethylase activity as well as both UDP-glucuronyl transferase and glutathione S-transferase activities. The increase of mutagenicity of DMBA observed in the Ames assay using hepatic microsomes from Sudan III-treated rats was inhibited by the addition of uridine 5'-diphosphoglucuronic acid or reduced glutathione with cytosol. Mutagenic metabolites of DMBA formed by CYP1A1 appeared to be effectively detoxified by these phase II enzymes. The results of this study suggest that Sudan III-induced prevention of in vivo mutagenesis is due to the induction of both CYP 1A1 and detoxifying phase II enzymes. The induced CYP1A1 may accelerate formation of active metabolic intermediates, but phase II enzymes are also induced and detoxify these intermediates to inactive metabolites. This would reduce residence time of the carcinogen in the body and the time of exposure to active metabolites for target organs.

7-Alkoxycoumarin O-Dealkylase↗