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Increasing industrial activity causes the release of chemical compounds into aquatic habitats, including toxic heavy metals like cadmium and medications like ketoprofen, posing considerable ecological concerns. Although previous studies have shown that cadmium and ketoprofen individually cause cognitive impairment, there is a lack of information on the combined neurological effects of the two substances. We investigated the neurological consequences of persistent cadmium exposure in the presence of ketoprofen on adult zebrafish, providing an essential model for understanding cumulative impacts on vertebrate organisms. Behavioral assessments, bioaccumulation rates, biochemical studies, and histopathological exams were conducted over 42 days in authentic environmental settings. The results of our study show that cadmium (10 µg/L) and ketoprofen (10 and 100 µg/L) at environmentally relevant concentrations had a significant impact on locomotor activity, social interactions, and cognitive responses, indicating cumulative neurotoxicity in co‐exposure groups compared to single pollutant groups. Biochemical tests show disturbances in antioxidant defense systems, while histological examinations reveal structural changes in zebrafish brain regions. Ketoprofen influences cadmium accumulation in the brain, underscoring the importance of conducting complete evaluations to understand the intricate interactions between environmental pollutants. This study improves our understanding of the complex interactions between heavy metals and medications, stressing the need to consider combined exposure when assessing the neurological effects on vertebrate models. [ABSTRACT FROM AUTHOR]

AbstractMosquito-borne diseases continue to pose significant threats to human populations, especially in developing and underdeveloped regions, where access to effective preventive measures remains limited. Mosquito repellents represent a cornerstone in the arsenal against these diseases, providing a barrier against mosquito bites. Mosquito repellents come in various formulations, including topical ointments and commercial vaporizers, with varying compositions. Common constituents include deodorized kerosene (DOK) as a solvent, pyrethroids, amides, essential oils for fragrance, and synergists. Despite their widespread use, the toxicological profiles of these repellents remain inadequately understood, raising questions about their safety in prolonged or excessive exposure scenarios. However, while their efficacy in preventing mosquito-borne illnesses is well-established, concerns persist regarding their potential toxicity to humans and the environment. This review critically examines the existing literature on the toxicity of mosquito repellents, focusing on their adverse effects on human health and environmental sustainability. Through an extensive analysis of available research, this review aims to shed light on the potential health risks associated with mosquito repellents, such as dermatological irritation, respiratory complications, and allergic reactions in humans. [ABSTRACT FROM AUTHOR]

Background and Purpose: Parkinson's disease (PD) is a prevalent neurodegenerative movement disorder characterized by motor dysfunction. Environmental factors, especially manganese (Mn), contribute significantly to PD. Existing therapies are focused on motor coordination, whereas nonmotor features such as neuropsychiatric symptoms are often neglected. Daidzein (DZ), a phytoestrogen, has piqued interest due to its antioxidant, anti‐inflammatory, and anxiolytic properties. Therefore, we anticipate that DZ might be an effective drug to alleviate the nonmotor symptoms of Mn‐induced Parkinsonism. Experimental Approach: Naïve zebrafish were exposed to 2 mM of Mn for 21 days and intervened with DZ. Nonmotor symptoms such as anxiety, social behaviour, and olfactory function were assessed. Acetylcholinesterase (AChE) activity and antioxidant enzyme status were measured from brain tissue through biochemical assays. Dopamine levels and histology were performed to elucidate neuroprotective mechanism of DZ. Key Results: DZ exhibited anxiolytic effects in a novel environment and also improved intra and inter fish social behaviour. DZ improved the olfactory function and response to amino acid stimuli in Mn‐induced Parkinsonism. DZ reduced brain oxidative stress and AChE activity and prevented neuronal damage. DZ increased DA level in the brain, collectively contributing to neuroprotection. Conclusion and Implications: DZ demonstrated a promising effect on alleviating nonmotor symptoms such as anxiety and olfactory dysfunction, through the mitigation of cellular damage. These findings underscore the therapeutic potential of DZ in addressing nonmotor neurotoxicity induced by heavy metals, particularly in the context of Mn‐induced Parkinsonism. [ABSTRACT FROM AUTHOR]

AbstractThe growing concern about pollution and toxicity in aquatic as well as terrestrial organisms is predominantly caused due to waterborne exposure and poses a risk to environmental systems and human health. This study addresses the co-toxic effects of cadmium (Cd) and ketoprofen (KPF), representing heavy metal and pharmaceutical discharge pollutants, respectively, in aquatic ecosystems. A 96-h acute toxicity assessment was conducted using zebrafish embryos. The results indicated that high dosages of KPF (10, 15, and 100 µg/mL) and Cd (10 and 15 µg/mL) reduced survivability and caused concentration-dependent deformities such as scoliosis and yolk sac edema. These findings highlight the potential defects in development and metabolism, as evidenced by hemolysis tests demonstrating dose-dependent effects on blood cell integrity. Furthermore, this study employs adult zebrafish for a 42-day chronic exposure to Cd and KPF (10 and 100 µg/L) alone or combined (10 + 10 and 100 + 100 µg/L) to assess organ-specific Cd and KPF accumulation in tissue samples. Organ-specific accumulation patterns underscore complex interactions impacting respiratory, metabolic, and detoxification functions. Prolonged exposure induces reactive oxygen species formation, compromising antioxidant defense systems. Histological examinations reveal structural changes in gills, gastrointestinal, kidney, and liver tissues, suggesting impairments in respiratory, osmoregulatory, nutritional, and immune functions. This study emphasizes the importance of conducting extensive research on co-toxic effects to assist with environmental risk assessments and safeguard human health and aquatic ecosystems. [ABSTRACT FROM AUTHOR]

AbstractIndustrial 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. [ABSTRACT FROM AUTHOR]