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The El Guájaro reservoir, situated in northern Colombia, holds significant economic and ecological importance. It is categorized as eutrophic due to factors such as wastewater discharges, agricultural practices, and the dragging of limestone material. These factors create favorable conditions for cyanobacterial proliferation. This study evaluates the diversity and abundance of cyanobacteria, with special attention to the genera identified as toxin producers, and bloom formers within the reservoir. Sampling was conducted in the photic zone at seven stations during both rainy and dry seasons between 2015 and 2019. Abundance and diversity were quantified using the iNEXT program, while a beta diversity analysis assessed community differentiation in relation to environmental parameters. A total of 86 species from 12 orders and 42 genera were identified, with 44% of these species noted as potentially toxic. A significant predominance of filamentous species was identified. Pseudanabaena and Phormidium were the most frequent and abundant genera. The results reveal distinct distribution and abundance patterns influenced by seasonal fluctuations. A notable bloom, co-dominated by Microcystis and Dolichospermum, occurred during the 2019 dry season, leading to the mortality of livestock and other animals. Urgent governance measures and control strategies are imperative to mitigate the health impact of such blooms.

Acetaminophen (APAP) is a widely used analgesic, especially for children. Its primary mechanism involves inhibiting cyclooxygenase enzymes and activating the endocannabinoid and TRPV1 systems. Though its toxicity is low, it can harm the liver in a dose-dependent manner. Low APAP doses can also increase pollutant-induced liver damage. Little is known about interactions between APAP and benzo[a]pyrene (B[a]P). This study aimed to assess if co-exposure to non-hepatotoxic doses of B[a]P and APAP causes liver injury in mice, exploring the underlying mechanisms. Female ICR mice received 50 mg/kg B[a]P or a vehicle for three days, followed by 200 mg/kg APAP or a vehicle. Liver injury was assessed through histopathological examination, serum transaminase activity, and gene expression analysis. In the B[a]P/APAP group, several histology changes were observed, including ballooning injury, steatosis, necrosis, inflammation, and apoptosis. Transaminase levels correlated with histopathological scores, and there was an increase in hepatic cytochrome P450 family 1 subfamily a member 1 (Cyp1a1) mRNA levels and a decrease in aryl hydrocarbon receptor (Ahr), cytochrome P450 family 2 subfamily e polypeptide 1 (Cyp2e1), superoxide dismutase 1 (Sod1), peroxisome proliferator activated receptor gamma (Ppar-γ), and caspase 3 (Casp3). This suggests that prior exposure to B[a]P makes mice more susceptible to APAP-induced liver injury, involving changes in gene expression related to metabolism, redox balance, and cell proliferation. Therefore, using therapeutic APAP doses after exposure to B[a]P could lead to liver injury. [ABSTRACT FROM AUTHOR]

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