Interconnected environmental challenges: heavy metal-drug interactions and their impacts on ecosystems.

Industrial expansion and inadequate environmental safety measures are major contributors to environmental contamination, with heavy metals (HMs) and pharmaceutical waste playing crucial roles. Their negative effects are most noticeable in aquatic species and vegetation, where they accumulate in tissues and cause harmful results. Interactions between HMs and pharmaceutical molecules result in the production of metal-drug complexes (MDCs), which have the potential to disturb diverse ecosystems and their interdependence. However, present studies frequently focus on individual pollutants and their effects on specific environmental parameters, leaving out the cumulative effects of pollutants and their processes across several environmental domains. To address this gap, this review emphasizes the environmental sources of HMs, elucidates their emission pathways during anthropogenic activities, investigates the interactions between HMs and pharmaceutical substances, and defines the mechanisms underlying the formation of MDCs across various ecosystems. Furthermore, this review underscores the simultaneous occurrence of HMs and pharmaceutical waste across diverse ecosystems, including the atmosphere, soil, and water resources, and their incorporation into biotic organisms across trophic levels. It is important to note that these complex compounds represent a higher risk than individual contaminants.

Skeletal and neurological risks demonstrated in zebrafish due to second-hand cigarette smoke and the neutralization of luteolin.

BACKGROUND: Cigarette smoke exposure poses significant health risks, including oxidative stress, inflammation, tissue damage, and neurodegenerative diseases. Luteolin, a natural flavonoid known for its antioxidant and anti-inflammatory properties, is of interest in countering these effects. AIM: This study aims to assess luteolin's protective potential against cigarette smoke extract (CSE) in adult zebrafish. MATERIALS AND METHODS: Adult zebrafish were exposed to CSE for 15 days, inducing smoke-related damage. Subsequent luteolin treatment assessed its impact. Evaluations included antioxidant enzymes (SOD, CAT), nitric oxide (NO), LDH activity (cellular damage), tissue integrity, fibrosis, amyloid plaque accumulation, and CSE component analysis via HPLC. KEY FINDINGS: CSE exposure heightened oxidative stress, reducing SOD and CAT activity and elevating NO levels, leading to cellular damage and tissue disruption, notably fibrosis and amyloid plaque accumulation. Inflammatory markers TNF-α and IL-1ß also increased. Luteolin treatment restored SOD and CAT activity, reduced LDH and NO activity, counteracting oxidative damage. It also mitigated fibrosis and reduced amyloid plaque deposition, preserving tissue integrity. Luteolin reduced TNF-α and IL-1ß levels and CSE components, displaying anti-inflammatory effects. SIGNIFICANCE: This study underscores luteolin's potential as a protective agent against cigarette smoke-induced harm in a zebrafish model.

Ophthalmic Intervention of Naringenin Decreases Vascular Endothelial Growth Factor by Counteracting Oxidative Stress and Cellular Damage in In Vivo Zebrafish.

Diabetes Mellitus is a metabolic disease that leads to microvascular complications like Diabetic retinopathy (DR), a major cause of blindness worldwide. Current medications for DR are expensive and report multiple side effects; therefore, an alternative medication that alleviates the disease condition is required. An interventional approach targeting the vascular endothelial growth factor (VEGF) remains a treatment strategy for DR. Anti-VEGF medicines are being investigated as the main therapy for managing vision-threatening complications of DR, such as diabetic macular oedema. Therefore, this study investigated the effect of flavonoid naringenin (NG) from citrus fruits on inhibiting early DR in zebrafish. When exposed to 130 mM glucose, the zebrafish larvae developed a hyperglycaemic condition accompanied by oxidative stress, cellular damage, and lipid peroxidation. Similarly, when adult zebrafish were exposed to 4% Glucose, high glucose levels were observed in the ocular region and massive destruction in the retinal membrane. High glucose upregulated the expression of VEGF. In comparison, the co-exposure to NG inhibited oxidative stress and cellular damage and restored the glutathione levels in the ocular region of the zebrafish larvae. NG regressed the glucose levels and cellular damage along with an inhibition of macular degeneration in the retina of adult zebrafish and normalized the overexpression of VEGF as a promising strategy for treating DR. Therefore, intervention of NG could alleviate the domestication of alternative medicine in ophthalmic research.