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Aim: Elevated levels of 16α‐hydroxyestrone (16α‐OHE1) have been described in endometrial cancer (EC) and estrogen receptors (ER) expressed in endometrial tissue, but research on their combined role is lacking. We aimed to investigate the affinity and binding specificity of EC antibodies against the 16α‐OHE1‐ERα aggregate in the serum of EC patients. Specificities of EC antibodies were also evaluated according to various clinical characteristics found in these cancer patients. Methods: The binding specificity and affinity of EC antibodies against 16α‐OHE1‐ERα in the serum of 120 EC patients were evaluated by direct binding and competition ELISA and quantitative precipitation titration. Binding of EC antibodies was also determined according to various clinical characteristics in EC patients through competition ELISA. Results: Antibodies from EC patients demonstrated high recognition of 16α‐OHE1‐ERα compared to ERα (P < 0.05) or 16α‐OHE1 (P < 0.001). The relative affinity of EC IgG was 1.49 × 10−7 M, 1.34 × 10−6 M and 1.13 × 10−6 M for 16α‐OHE1‐ERα, ERα and 16α‐OHE1, respectively. Several factors, such as obesity, postmenopausal status, use of hormonal therapy, ER and progesterone receptor (PR) status, low 2‐OHE1/16α‐OHE1 ratio, chemotherapy and hypertension, augment the production of antibodies against 16α‐OHE1‐ERα in EC patients. Conclusion: 16α‐OHE1‐ERα is a high‐affinity antigen for EC antibodies in the serum of EC patients and might function as a biomarker for this disease. Furthermore, several factors enhanced the production of antibodies against 16α‐OHE1‐ERα in the sera of these EC patients. [ABSTRACT FROM AUTHOR]

Abstract Mentally depressed breast cancer (MDBC) patients expressed estrogen receptor (ER) and 16α‑hydroxyestrone (16α‑OHE 1) is directly responsible for causing breast cancer (BC). This study aimed to identify whether depression in breast cancer patients enhanced the production of autoantibodies against 16α‑OHE 1 -ER adduct in breast cancer patients. The antibodies in the serum of 65 breast cancer patients (including 35 MDBC) and 40 control subjects were screened by direct binding, inhibition enzyme-linked immunosorbent assay (ELISA), and quantitative precipitin titration. Competition ELISA was also utilized for the estimation of 16α‑OHE 1 in the serum of 30 cancer patients. Autoantibodies from MDBC showed strong recognition to 16α‑OHE 1 -ER in comparison to overall breast cancer patients (p < 0.05) and control subjects (p < 0.001). Although breast cancer sera showed high binding to 16α‑OHE 1 -ER in comparison to ER (p < 0.05) or 16α‑OHE 1 (p < 0.001), the relative affinities of autoantibodies for 16α‑OHE 1 -ER were found to be 1.38 × 10−7 and 1.23 × 10−7 for breast cancer and MDBC patients respectively. No significant difference, either in the level of 16α‑OHE 1 or 2‑hydroxyestrone/16α‑OHE 1 ratio, was observed in the serum of cancer patients compared with controls, although inflammatory cytokines (IL-6, TNF-α) were significantly high in these patients. Depression in breast cancer patients augments the production of autoantibodies against 16α‑OHE 1 -ER through the generation of inflammatory conditions. Depression in these patients increased the release of pro-inflammatory cytokines that generate more autoantibodies and show strong binding with 16α‑OHE 1 -ER. Highlights • Depression increases autoantibodies production in breast cancer through inflammatory conditions. • Depression increases the release of inflammatory cytokine in breast cancer. • 16α‑Hydroxyestrone and estrogen receptor generate neo-epitopes, well recognized by breast cancer patient's IgGs. [ABSTRACT FROM AUTHOR]

Milk and dairy products are one of the chief sources of nutrition for human beings particularly for infant and children. Aflatoxin M1 (AFM1) a hydroxylated metabolite of aflatoxin B1 found in milk and milk products causes serious health issues for human beings. The objective of this study was to evaluate the effect of storage on the level of aflatoxin M1 in milk and other dairy products sold at retail stores of Tripoli Province, Libya. Selected samples (Skimmed and cream milk, infant milk formula, butter, cheese, Cheddar, spread and slice) were evaluated by using specialized RIDASCREEN AFM1 competitive enzyme linked immune sorbent assay (ELISA) technique. Our investigation revealed that, the concentration of AFM1 increased with the duration of storage. Furthermore, we found that the newly manufactured samples had very low concentration of AFM1 and within the permitted range. Moreover, AFM1 concentration in skimmed and cream milk having 6 month shelf life had 5.00 ngkg-1 and 5.03 ngkg-1 respectively. Furthermore, both the expired skimmed and cream milk had AFM1 concentrations 121.8 ngkg-1 and 108.18 ngkg-1, respectively. In addition to that, we found that the levels of AFM1 in different dairy products varies with different shelf lives (12 and 1 month), such as cheddar (5.0 and 72.79 ngkg-1), Spread (5.30 and 60.03 ngkg-1), Slice (5.50 and 61.18 ngkg-1). Additionally, infant milk formula with shelf life of 24 months and expired samples had AFM1 less than 5.00 ngkg-1 and 60.8 ngkg-1, respectively. Based on our investigation, we found that the presence AFM1 in milk and milk products at high concentration may cause serious illness to consumers' health and the consequent economic losses. [ABSTRACT FROM AUTHOR]

• Depression linked to higher antibodies production against estogenized insulin in T1D. • Depression enhance the release of IL-1β and IL-17 in T1D. • Depression generates inflammatory conditions in T1D. Depression has been commonly associated with type 1 diabetes (T1D) and insulin covalently modified with catecholestrogens (CEs) was found in serum of these T1D patients. This study aimed to know whether depression link to higher antibodies against estrogenized insulin in T1D. ELISA (direct binding and competition) and quantitative precipitin titration were used to detect antibodies and their affinities against estrogenized insulin in the serum of 66 depressed T1D (DT1D) patients (out of 110 T1D) and 41 control subjects. Antibodies from DT1D patients showed high binding specificity to estrogenized insulin (2-hydroestradiol-insulin; 2-OHE 2 -Ins) in comparison to overall T1D patients (p < 0.05) or control subjects (p < 0.001). However, T1D sera demonstrate high recognition to 2-OHE 2 -Ins as compared to Ins (p < 0.05) or 2-OHE 2 (p < 0.001). The affinity of antibodies from DT1D and T1D patients was 1.32 × 10-7 M and 1.43 × 10-7 M, respectively. Depression linked to higher antibodies production against estrogenized insulin in T1D. Furthermore, depression in T1D generates inflammatory conditions that further increased antibodies production in T1D patients. [ABSTRACT FROM AUTHOR]

Insulin (Ins) covalently modified by catecholestrogens (CEs) was commonly found in diabetic patients who have developed insulin resistance. Estrogenization of insulin altered its molecular function and effect carbohydrates metabolisms in these patients. Insulin resistance is a common phenomenon in diabetes but the exact mechanism remains unknown. In this study, binding specificity and affinity of autoantibodies against estrogenized insulin (4-hydroxyestradiol-insulin; 4-OHE 2 -Ins) were assayed in the serum of type 1 diabetes (T1D) patients in order to explain the phenomena behind insulin resistance. Specificity and affinity of autoantibod i es from the sera of 66 T1D patients and 41 controls were analyzed by direct binding, competition ELISA and quantitative precipitin titration. Insulin was also estimated in the serum of T1D patients by ELISA. Estrogenized insulin (4-OHE 2 -Ins) exhibited high affinity and specificity to T1D autoantibodies in comparison to Ins (p <.05) or 4-OHE 2 (p <.001). Estrogenization of insulin alters its interaction with the insulin receptor (IR). The affinity constant of 4-OHE 2 -Ins with the T1D autoantibodies was found to be 1.41 × 10−7 M. Estrogenization of insulin by catecholestrogen makes these molecules highly antigenic and produced high - affinity autoantibodies in T1D patients. As a result, patients develop insulin resistance and presented this molecule as a potential biomarker for T1D. • Estrogenized insulin (4-OHE 2 -Ins) exhibited high affinity and specificity for T1D autoantibodies. • Estrogenization of insulin alters the normal functions of the insulin in T1D patients • Estrogenization of insulin in the blood produced autoantibodies; as a result insulin resistance is developed in T1D patients [ABSTRACT FROM AUTHOR]

Depression is the common and early symptoms associated with early onset of SLE, 16α-hydroxyestrone (16α-OHE 1) levels were found to be significantly higher in serum and urine in patients with SLE. This study was carried out in order to know whether depression and its related parameters in the SLE patients enhanced the production of autoantibodies against 16α-OHE 1 -albumin (A) complexes. The autoantibodies in the serum of 100 SLE [including 65 depressed SLE (DSLE)] patients and 37 control subjects were detected by using direct binding, inhibition ELISA and quantitative precipitin titration. Autoantibodies from DSLE patients (and also the patients who were taken anti-depressant and with neurological symptoms) showed high binding to 16α-OHE 1 -A in contrast to SLE (p < 0.05) and control subjects (p < 0.001). Although, SLE sera showed high recognition to 16α-OHE 1 -A in comparison to A (p < 0.05) or 16α-OHE 1 (p < 0.001). The affinity of autoantibodies for 16α-OHE 1 -A was found to be high for DSLE (1.16 × 10−7 M) and SLE (1.24 × 10−7 M) patients as detected by Langmuir plot. The concentration of 16α-OHE 1 (p < 0.05) and inflammatory cytokines (IL-6, p < 0.05 and IL-17, p < 0.001) in the serum of SLE patients was found to be significantly higher than controls. Depression and its related parameters in SLE enhanced the production of autoantibodies against 16α-OHE 1 -A through the generation of inflammatory conditions. Depression in SLE patients increased the release of pro-inflammatory cytokine (IL-6 and IL-17) that in turn generating more autoantibodies and showed strong recognition to 16α-OHE 1 -A. • Depression and its related parameters increase the production of SLE autoantibodies through inflammatory conditions. • They increase the release of inflammatory cytokine (IL-6 and IL-17) in SLE patients. • 16α-Hydroxyestrone and albumin generate unique epitopes, well recognized by SLE autoantibodies. [ABSTRACT FROM AUTHOR]