The mechanisms of microcystin-LR-induced genotoxicity and neurotoxicity in fish and mammals: Bibliometric analysis and meta-analysis

Abstract

Microcystin-leucine arginine (MC-LR) is a typical cyanobacterial toxin, and the threat of this toxin is increasing among organisms. Despite extensive toxicological studies on MC-LR, there is no comprehensive analysis based on previously published data. Therefore, we conducted bibliometric analysis and meta-analysis to identify research hotspots and to elucidate the key mechanism of the relationship between MC-LR and genotoxicity and neurotoxicity among fish and mammals. One of the hotspots is toxic mechanisms (indicated by the frequent appearance of oxidative stress, DNA damage, apoptosis, neurotoxicity, genotoxicity, ROS, comet assay, signalling pathway, and gene expression indicate as keywords). The density visualization shows a high frequency of “microcystin-LR” and “toxicology,” and the overlay visualization emphasizes the prominence of “neurotoxicity” in recent years. These findings confirm the importance of studying MC-LR toxicity. Meta-analysis indicated that in both fish and mammals, MC-LR exposure increased ROS levels by 294 % and increased DNA damage biomarkers by 174 % but decreased neurotoxicity biomarkers by 9 %. Intergroup comparisons revealed that the exposure concentration of MC-LR was significantly correlated with genotoxicity and neurotoxicity levels in both fish and mammals (p < 0.05). Furthermore, the random forest (RF) model revealed that exposure concentration was the primary determinant associated with the induction of ROS, genotoxicity, and neurotoxicity induced by MC-LR. This is likely the dominant mechanism by which excessive ROS production induced by MC-LR causes oxidative stress, ultimately leading to genotoxicity and neurotoxicity in both fish and mammals.