al-turath Medical Journal

Background: The neuroendocrine and immune systems operate as deeply integrated regulatory networks, jointly modulating host responses to infectious agents and metabolic perturbations. Disruptions in the hypothalamic-pituitary-adrenal (HPA) axis frequently coincide with pathological oxidative stress, creating a self-amplifying cycle of immunological dysfunction, hormonal imbalance, and cellular damage. Emerging evidence further implicates mitochondrial dysfunction, ferroptosis, and immunometabolic reprogramming as critical mechanistic intermediaries.

Objective: This review critically examines the bidirectional relationship between immunoendocrine signaling and oxidative stress across infectious and metabolic diseases, with emphasis on the Nrf2/NF-κB axis, NLRP3 inflammasome, ferroptosis, immunometabolic reprogramming, and the microbiome-endocrine-immune interface.

Key Findings: Cortisol, thyroid hormones, melatonin, and insulin orchestrate pro- and anti-inflammatory immune activity. ROS generated during infection and metabolic disease amplify cytokine cascades, impair antioxidant enzyme systems (SOD, CAT, GPx), and suppress endocrine feedback loops. Mitochondrial ROS trigger NLRP3 inflammasome activation, while ferroptosis—an iron-dependent, GPX4-regulated cell death pathway—emerges as a critical tissue injury mechanism in diabetes and severe infections. The Warburg-shifted immunometabolic reprogramming of activated immune cells further amplifies inflammatory cascades.

Conclusion: Multi-target therapeutic strategies simultaneously addressing endocrine dysregulation, ferroptosis, mitochondrial dysfunction, and oxidative burden represent the most promising approach for managing complex infectious and metabolic pathologies. Sex-stratified multiomics investigations and AI-assisted biomarker integration are urgently needed.

Background: Type 2 diabetes mellitus (T2DM) is defined by persistent hyperglycemia which leads to oxidative stress and low-grade inflammation which causes microvascular complications. The interconnection between inflammatory signs, oxidative stress, and glycemic control is imperative to understanding of patients at risk. Purpose: The purpose of the study was to compare inflammatory (IL-6, TNF-a, hs-CRP) and oxidative stress (MDA, TAC, SOD) parameters between T2DM patients and healthy controls and determine the relationship between them and microvascular complications and glycemic control. Methods: 150 T2DM patients (75 with complications, 75 without complications) and 50 healthy controls were involved in this case-control study. Blood samples were fasted and compared in terms of HbA1c, fasting glucose, lipids profile, inflammatory (IL-6, TNF-a, hs-CRP), and oxidative stress (MDA, TAC, SOD) levels. The analysis of the predictive performance to complications was done using receiver operating characteristic (ROC) analysis. Findings: IL-6 (18.4+-4.2 vs 4.2+-1.1 pg/mL, P<0.001), TNF-a (28.6+-6.4 vs 8.4+-2.1 pg/mL, P<0.001), hs-CRP (6.8+-1.8 vs 1.2+-0.4 mg/L, P<0.001) were found to be significantly higher in T2DM patients than controls. The level of oxidative stress was high: the MDA level doubled, and the TAC fell by 48%. Further increases in IL-6 (24.6+-5.8 vs 12.4+-3.2 pg/mL, P<0.001) and MDA (8.4+-2.1 vs 4.8+-1.2 nmoI/mL, P<0.001) were found in patients with complications. The highest predictive accuracy of microvascular complications was IL-6/TAC ratio (AUC=0.92). Conclusion: There is a great increase of inflammatory and oxidative stress markers in T2DM patients, and additional increases in microvascular complication patients. The IL-6/TAC ratio can be used as an effective biomarker to detect patients with a risk of complications.

Background: Myocardial infarction (MI) is a life-threatening condition associated with coronary artery disease. Early, rapid, and accurate diagnosis plays a critical role in reducing mortality rates. Therefore, clinicians rely on a range of biomarkers for the early detection of myocardial injury, including copeptin. This study aimed to evaluate the correlation between copeptin levels, lipid profile abnormalities, and kidney function parameters in patients with myocardial infarction.Methods: This study was conducted from July 2025 to November 2025 and included 90 male participants. The first group consisted of 60 patients diagnosed with myocardial infarction (MI), while the second group included 30 apparently healthy individuals as controls. Participants’ ages ranged from 50 to 70 years. Inclusion criteria involved patients attending or admitted to Samarra General Hospital and diagnosed with MI by a specialist physician. Exclusion criteria included patients with cancer, hepatitis, or renal failure.Results: The findings of the current study revealed a significant increase (P ≤ 0.05) in serum copeptin levels in MI patients, reaching (13.99 ± 2.95 pg/ml). Lipid profile analysis demonstrated significant elevations (P ≤ 0.05) in total cholesterol (260.2 ± 23.9 mg/dl), triglycerides (147.3 ± 33.4 mg/dl), low-density lipoprotein cholesterol (LDL-C) (162.4 ± 26.9 mg/dl), and very low-density lipoprotein cholesterol (VLDL-C) (29.46 ± 6.69 mg/dl) in MI patients. In contrast, high-density lipoprotein cholesterol (HDL-C) levels showed a significant decrease, reaching (68.4 ± 14.7 mg/dl). Furthermore, the study demonstrated significant increases in urea (6.32 ± 1.210 mg/dl), uric acid (8.43 ± 2.13 mg/dl), and creatinine (1.048 ± 0.331 mg/dl) levels in MI patients. A strong positive correlation was observed between copeptin and both urea (r = 0.550) and creatinine (r = 0.438). However, very weak correlations were found between copeptin and uric acid as well as lipid profile parameters. Conclusion:* The present study suggests that copeptin can be used as a reliable biomarker in myocardial infarction, as its levels significantly increase in affected patients. Additionally, lipid profile components and kidney function parameters (urea, uric acid, and creatinine) were significantly elevated, while HDL-C levels were significantly reduced in MI patients. A strong positive correlation exists between copeptin and both urea and creatinine, whereas its correlation with uric acid and lipid profile is very weak.

Background: Cadmium (Cd) is a heavy metal that is toxic and accumulates mainly in the liver and kidney, resulting in plants being severely damaged due to oxidative stress, inflammation and hormonal imbalance. Cadmium toxicity, though efforts are being put to control human exposures, is one of the biggest health problems in majority of the regions in the world like Iraq. Purpose: The aim of the study was to evaluate the ability of nano-curcumin (NC) to prevent the liver and kidney damages caused by cadmium chloride (CdCl 2 ) in male Wistar rats with a focus on the oxidative stresses, inflammatory cytokines and hormones. Procedures: The forty adult males (n = 40) were divided into four equal groups (n = 10) to take the number of Wistar rats. Normal saline was used to spray group I (control). Eight weeks later group II was administered CdCl 2 (5 mg/kg body weight, orally, daily). The group III was administered with nano-curcumin (orally, 50mg/kg body weight, every day) within a period of eight weeks. Group IV- an intervention that was done on them to have CdCl 2 and nano-curcumin simultaneous in the same doses over eight weeks. At the conclusion of the experiment, blood and tissue samples were analyzed and examined using the markers of liver (ALT, AST, ALP, total bilirubin, total protein, albumin), kidney (creatinine, urea, BUN, uric acid, total cholesterol, triglycerides) functioning and oxidative stress (MDA, SOD, CAT, GPx, GSH, TAC. Results: The liver enzymes, kidney functioning markers, MDA, inflammatory cytokines and cortisol levels significantly increased in Group II and significantly decreased when compared to control group (p < 0.05). All these parameters were also significantly (p < 0.05) increased by Group IV treated with the co-treatment with nano-curcumin compared to Group II however not returning to the normal values. Conclusion: Nano-curcumin was discovered to possess immense protective effects against cadmium-induced liver and kidney damage in male rats because it was able to alleviate oxidative stress, decrease the levels of inflammatory cytokines and help in normalization of hormone levels. These results suggest that nano-curcumin can be a natural compound potentially exhibiting good outcomes in alleviating the negative effects of heavy metal toxicity.