Zinc, lead, and cadmium levels in serum and milk of lactating women in Ibadan, Nigeria.

Zinc (Zn) is known to interact with lead (Pb) and cadmium (Cd) reversing their toxicity and reducing their concentrations. However, lactating women are at high risk of developing Zn deficiency, which may result in Pb and Cd intoxication or increased exposure of breast-fed infants to Pb and Cd from breast milk. The aim of this study was to determine Zn, Pb, and Cd concentrations and examine their relationship in serum and breast milk of lactating women in Ibadan, Nigeria. Ninety-two lactating women were recruited into this study. Anthropometric measurements were assessed by standard methods while serum and breast milk concentrations of Zn, Pb, and Cd were assessed by atomic absorption spectrophotometry. Data analyzed statistically by Student's t test, Pearson's correlation coefficient, and a multiple regression model were significant at p < 0.05. Zn deficiency was observed in 12 (17.1%) of lactating women. Breast milk levels of Zn, Pb, and Cd were significantly higher than their levels in serum, whereas the ratios Zn:Pb and Zn:Cd in milk were significantly less than serum ratios. Significant negative correlation was observed between milk Pb and serum Zn:Pb while milk Cd correlated positively with milk Zn. Significant positive correlations were observed between serum Zn and serum Zn:Pb, serum Zn and serum Zn:Cd, as well as serum Zn:Cd and serum Zn:Pb. Serum Cd and serum Zn were significantly negatively related. Significant negative correlations between serum Pb and serum Zn:Pb as well as milk Zn:Pb. Serum Cd and serum Zn:Pb as well as serum Zn:Cd correlated negatively. Milk Cd and Zn/Cd positively related with milk Pb while milk Zn was a negatively related with milk Pb in a multiple regression model ( R2 = 0.333; p = 0.023). Breast milk may be contaminated by toxic metals. However, Zn supplementation in deficient mothers may protect maternal and infant health.

Cytokine profile in Nigerians with tubal infertility.

INTRODUCTION: Immune response to genital Chlamydia trachomatis infection is involved in both immunity and pathology. The cytokine profile during infection has been implicated in the disease outcome, either resolution or severe sequelae. Serum cytokines of Chlamydia positive Nigerian women with tubal infertility were assessed to determine their possible relationship with tubal occlusion. MATERIAL AND METHODS: One hundred and fifty age-matched consenting women (100 fertile and 50 with tubal infertility) were recruited based on C. trachomatis antibody positivity and grouped into infertile Chlamydia positive (CTpos) women (n = 50), fertile Chlamydia positive women (n = 50) and fertile Chlamydia negative (CTneg) women as controls (n = 50). High vaginal swabs and endo-cervical swabs were collected for microscopy, culture and gram staining. Cytokines [transforming growth factor ß1 (TGF-ß1), interferon γ (IFN-γ), tumor necrosis factor α (TNF-α), interleukin (IL)-4, IL-10 and IL-17A] were estimated by ELISA in sera. Data were analyzed using ANOVA, χ (2) and Spearman's correlation at p = 0.05. RESULTS: Lower IFN-γ levels were observed in infertile women compared to fertile women. Fertile CTneg women had significantly higher TNF-α, and TGF-ß1 compared to fertile and infertile CTpos women, respectively. Lower IL-10 levels were seen in fertile CTpos women compared to the infertile CTpos group. Vaginal discharge was negatively correlated with TNF-α and IFN-γ and positively with IL-4 in Chlamydia positive women. CONCLUSIONS: Chlamydia positive women with tubal infertility have higher IL-10 and lower IFN-γ levels than controls, which may contribute to their development of tubal pathology.

Pituitary, Gonadal, Thyroid Hormones and Endocrine Disruptors in Pre and Postmenopausal Nigerian Women with ER-, PR- and HER-2-Positive and Negative Breast Cancers.

Breast cancer is broadly sub-divided into hormone responsive and non-hormone responsive subtypes. Estradiol has been associated with hormone responsive breast cancers. There is, however, a paucity of information on the role of sex hormones, gonadotropins, and thyroid hormone in non-hormone responsive breast cancer. This study aimed to determine differences in the serum levels of sex hormones, gonadotropins, thyroid hormones, and endocrine disruptors (lead, cadmium, and arsenic) in Nigerian women with hormone responsive and non-hormone responsive breast cancers. Seventy-nine non-pregnant women aged 28⁻80 years with histologically confirmed breast cancer were recruited, pre-therapy, into this cross-sectional study. They comprised 52 premenopausal women and 27 postmenopausal women recruited from the Surgical Oncology Clinic of the Department of Surgery, University College Hospital, Ibadan. Comparison of biochemical parameters were based on the positivity (+) and negativity (-) of estrogen receptor (ER), progesterone receptor (PR) and human epithelial receptor-2 (HER-2). Estradiol, progesterone, follicle stimulating hormone (FSH), luteinizing hormone (LH), free thyroxine (FT4), free triiodothyronine (FT3), and thyroid stimulating hormone (TSH) were determined using enzyme immunoassay (EIA). Serum lead, cadmium and arsenic were determined using atomic absorption spectrophotometry (AAS). Expression of ER, PR and HER2 were determined using immunohistochemistry. Data was analyzed using Mann-Whitney U-test and multiple regression, with p < 0.05 considered as being statistically significant. Estradiol and progesterone were significantly higher in breast cancer participants with ER- and PR- compared with those with ER⁺ and PR⁺ breast cancer (p < 0.05). Follicle stimulating hormone and LH levels were significantly higher in participants with ER⁺ and PR⁺ breast cancer compared with participants with ER- and PR- breast cancer (p < 0.05). Arsenic was inversely related with TSH in premenopausal participants with ER- and PR- (ß = -0.305; ß = -0.304, respectively). Sex hormones and gonadotropins appear to be involved in the pathogenesis of triple negative and luminal breast cancer, respectively.

Male Sexual Dysfunction, Leptin, Pituitary and Gonadal Hormones in Nigerian Males with Metabolic Syndrome and Type 2 Diabetes Mellitus.

BACKGROUND: Pituitary and gonadal dysfunctions resulting from increased adiposity leading to disturbances of sexual and reproductive functions have been reported in males with metabolic syndrome (MS) and type 2 diabetes mellitus (DM2). The aim of this study was to evaluate sexual dysfunction, leptin, and reproductive hormones in Nigerian males with MS and DM2. METHODS: Participants were 104 men (34 males with DM2, 17 men with MS and 53 men with normal body mass index (18.5-24.9 Kg/m (2)) without MS (controls)). The International Diabetes Federation (2005) criteria were used for MS diagnosis. Reproductive history, anthropometry, blood pressure (BP) and 10 ml fasting blood samples were obtained by standard methods. Fasting plasma glucose, total cholesterol, triglycerides and high density lipoprotein cholesterol were determined by enzymatic methods while low density lipoprotein cholesterol was calculated. Leptin, follicle stimulating hormone (FSH), luteinising hormone (LH), prolactin, testosterone and oestrogen were determined by enzyme immunoassay (leptin by Diagnostic Automation, Inc.; others by Immunometrics (UK) Ltd.) while oestrogen-testosterone ratio was calculated. Data analyzed using ANOVA, Chi square and multiple regression were statistically significant at p<0.05. RESULTS: Testosterone was significantly lower in MS than controls while oestradiol and ETR were significantly higher in MS compared with controls and DM2 group (p<0.05). ETR significantly predicted testosterone in all groups (p<0.05). Significantly lower libido was observed in men in MS than controls and DM2 groups (p<0.05). CONCLUSION: Sexual and reproductive dysfunction may be related to increased conversion of testosterone to oestrogen in increased adipose mass in men with metabolic syndrome and type 2 diabetes mellitus.

Female reproductive hormones and biomarkers of oxidative stress in genital Chlamydia infection in tubal factor infertility.

BACKGROUND: Genital Chlamydia infection (GCI) and the associated pathologies have been implicated in tubal infertility. Though the actual pathologic mechanisms are still uncertain, oxidative stress and other factors have been implicated. The purpose of the study was to determine the possible contribution of female reproductive hormones and biomarkers of oxidative stress in genital Chlamydial infection to tubal occlusion. METHODS: This prospective case control study was carried out by recruiting 150 age matched women grouped into infertile Chlamydia positive women (n = 50), fertile Chlamydia positive women (n = 50) and fertile Chlamydia negative women as controls (n = 50). High vaginal swabs and endocervical swabs were collected for screening Neisseria gonorrhoeae, Chlamydia trachomatis, Trichomonas vaginalis, Treponema pallidum, Staphylococcus aureus, and Candida albicans. Sera were collected for estimation of Chlamydia trachomatis antibody, female reproductive hormones [Follicle Stimulating Hormone (FSH), Luteinizing Hormone (LH), Oestradiol (E2), Progesterone (P4), Prolactin (PRL)] and biomarkers of oxidative stress [Total Antioxidant Capacity (TAC) and 8-hydroxyl-2-deoxyguanosine (8-OHdG)] by enzyme immunoassay (EIA). Data were analyzed using chi square, analysis of variance and LSD Post hoc to determine mean differences at p = 0.05. RESULTS: Among women with GCI, higher levels of LH and 8-OHdG were observed in infertile Chlamydia positive women compared to fertile Chlamydia positive women (p < 0.05). Higher levels of LH and 8-OHdG and lower TAC levels were observed in infertile Chlamydia positive women compared to fertile Chlamydia negative controls (p < 0.05). CONCLUSION: Mechanisms including oxidative DNA damage and reduced antioxidant capacity may be involved in the pathology of Chlamydia induced tubal damage.