The toxic footprint of lead exposure: oxido-inflammatory biomarkers in urban populations of Niger Delta, Nigeria

Occupational Organophosphorus Pesticide Exposure and Metabolic Syndrome: Implications of PPARγ

Organophosphorus pesticides (OPPs) are widely used and have recently been linked to metabolic syndrome (MS). This study aimed to investigate the probable association between chronic OPP exposure and MS among farm workers in Sharkia Governorate, Egypt, and to assess the potential role of peroxisome proliferator-activated receptor gamma (PPARγ). This comparative cross-sectional study included 140 participants, equally divided into OPP-exposed farm workers and non-exposed subjects. OPP exposure was confirmed by detecting plasma residues and cholinesterase activity. MS was diagnosed by assessing body mass index (BMI), waist circumference (WC), blood pressure, plasma glucose, serum insulin, and lipid parameters. Oxidative and inflammatory markers, including malondialdehyde (MDA), gamma-glutamyl transferase (GGT), ferritin, superoxide dismutase (SOD), tumor necrosis factor-alpha (TNF-α), and high-sensitivity C-reactive protein (hs-CRP), were measured. The mRNA expression of the PPARγ and paraoxonase 1 (PON1) genes was also investigated. In total, 60% of farm workers demonstrated MS, compared with 10% of non-exposed participants. Workers exhibited elevated oxidative and inflammatory indices and reduced PPARγ and PON1 expression. PPARγ positively correlated with high-density lipoprotein (HDL), SOD, and PON1, while negatively correlating with glucose, insulin resistance (IR), low-density lipoprotein (LDL), triglycerides (TGs), MDA, GGT, ferritin, TNF-α, and hs-CRP. The study concluded that chronic OPP exposure was associated with increased oxidative stress and inflammation, reduced PPARγ and PON1 expression, disturbed glucose and lipid metabolism, and increased IR. The observed associations between PPARγ downregulation, metabolic disturbances, and oxidative and inflammatory markers suggest that PPARγ dysregulation may represent a potential mechanistic link between chronic OPP exposure and MS. However, this proposed mechanism requires further validation.

THE ROLE OF OXIDATIVE STRESS BIOMARKERS IN ANIMAL HEALTH, TOXICOLOGY, AND ENVIRONMENTAL MONITORING

The oxidative stress biomarkers have gained significance in veterinary medicine, animal production, toxicology and environmental biomonitoring because of their link between redox imbalance and clinically as well as ecologically relevant results. RONS are produced during metabolism, immune defence, reproduction, growth and adaptation but excess production or a lack of antioxidants can lead to damage of lipids, proteins, DNA, mitochondria and cellular membranes. This review includes an integrated biomarker framework, practical interpretation criteria and original explanatory diagrams which detail the use of oxidative stress markers within animal health, toxicological evaluation and environmental monitoring, incorporating a One Health perspective. The biomarkers reviewed are those involved in lipid peroxidation (malondialdehyde), antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase), and molecular damage markers (protein carbonyls and 8-hydroxy-2'-deoxyguanosine). The oxidative stress biomarkers reviewed in this report are not diagnostic biomarkers of their own, but rather are indicators of early warning and should be combined with pathology, performance indicators, contaminant data and longitudinal surveillance.

Serum Molecular Fingerprints of Oxidative Stress Underlying Neurocognitive and Motor Dysfunction in Pesticide‐Exposed Populations

We investigated the relationship between chronic pesticide exposure, oxidative stress, and neurocognitive alterations in rural populations of Celendín, Cajamarca, Peru. A total of 101 adults (18–86 years) were evaluated through neuropsychological (NEUROPSI) and neuromotor assessments, serum oxidative stress biomarkers, and Fourier‐transform infrared spectroscopy (FT‐IR) of serum samples. Biomarkers analyzed included superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), total glutathione, lipid peroxidation (malondialdehyde), biopyrrins (BPn), and 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG). Statistical comparisons (Mann–Whitney U) and multivariate analyses (PCA, PLS‐DA) were performed to identify biochemical and spectral alterations. Pesticide users exhibited a significantly higher frequency of attention deficit (OR = 4.4, 95% CI = 1.2–15.9) and elevated serum 8‐OHdG levels (p = 0.042), indicating increased oxidative DNA damage. While antioxidant enzyme activities did not differ significantly, higher malondialdehyde and BPn levels suggested enhanced lipid and bilirubin oxidation. FT‐IR analysis revealed distinct spectral signatures in individuals with moderate cognitive impairment, impaired left‐hand motor control, and executive dysfunction (calculation). Significant bands appeared in the 440–493 cm−1 region (disulfide/polysulfide bonds), 2573 cm−1 (thiols), and 3630–3840 cm−1 (free hydroxyl groups), consistent with oxidative protein and glycan modifications. Additional signals between 2089 and 2255 cm−1 suggested carbamylation‐related isothiocyanate and cyanate groups. These findings suggest that oxidative stress is a key mechanism underlying pesticide‐related neurocognitive dysfunction. Combining oxidative stress biomarkers with FT‐IR provides a rapid, minimally invasive approach for identifying serum molecular fingerprints with potential applications in screening and monitoring pesticide‐induced neurotoxicity.

Effects of sub-acute aluminium phosphide exposure on hepatorenal biomarkers and antioxidant defense in rats.

Investigating the dose-dependent toxicity of AlP on biochemical biomarkers, antioxidant defense responses, and histological changes in rat liver and kidneys found sub-acute AlP exposure caused dose-dependent liver and kidney toxicity, high doses induced pronounced damage, and low doses showed mild or minimal effects.

Safranal Attenuates Malathion-Induced Oxidative Stress and AChE Inhibition Across Blood, Hepatic, Renal, and Brain Matrices

Organophosphate pesticides, particularly malathion, are widely used in agriculture but pose severe toxicity risks to non-target organisms through acetylcholinesterase (AChE) enzyme inhibition and the induction of oxidative stress. This study investigated the potential protective effects of safranal, a primary bioactive component of saffron (Crocus sativus L.) known for its antioxidant and anti-inflammatory properties, against malathion-induced systemic and tissue-specific toxicity. Experimental groups were evaluated by measuring malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and GPx (glutathione peroxidase) levels, alongside AChE enzyme activity in the blood, liver, kidney, and brain tissues. The findings demonstrated that malathion exposure caused profound toxicity characterized by severe AChE inhibition, accelerated lipid peroxidation, elevated NO levels, and a critical depletion of both enzymatic and non-enzymatic antioxidant defenses across all analyzed matrices. Conversely, safranal administration served as an effective therapeutic intervention. It mitigated oxidative damage, limited the exhaustion of key antioxidant enzymes by reducing reactive oxygen species, and supported the preservation of AChE functionality. Notably, safranal’s protective efficacy exhibited tissue-dependent variations; while it significantly attenuated oxidative stress markers and preserved cellular viability in the plasma, liver, and renal matrices, it demonstrated limited protective capacity in brain tissue under the current experimental conditions. In conclusion, safranal represents a promising bioactive countermeasure against organophosphate-induced systemic injury. However, further research is warranted to elucidate its precise transport mechanisms and potential limitations in crossing the blood-brain barrier.

Molecular Epidemiology, Hematobiochemical Alterations, and Oxidative Stress-Induced Genotoxicity of Equine Trypanosomiasis in Pakistan