Rhodamine B, an organic environmental pollutant induces reproductive toxicity in parental and teratogenicity in F1 generation in vivo.

This study investigated the reproductive toxicity of rhodamine B in zebrafish and its transgenerational effects on the F1 generation. In silico toxicity predictions revealed high toxicity of rhodamine B, mainly targeting pathways associated with the reproductive and endocrine systems. In vivo experiments on zebrafish demonstrated that rhodamine B exposure at a concentration of 1.5 mg/L led to significant impairments in fecundity parameters, particularly affecting females. Histopathological analysis revealed distinct changes in reproductive organs, further confirming the reproductive toxicity of rhodamine B, with females being more susceptible than males. Gene expression studies indicated significant suppression of genes crucial for ovulation in rhodamine B-treated female fish, highlighting hormonal imbalance as a potential mechanism of reproductive toxicity. Furthermore, bioaccumulation studies showed the presence of rhodamine B in both adult fish gonads and F1 generation samples, suggesting transgenerational transfer of the dye. Embryotoxicity studies on F1 generation larvae demonstrated reduced survival rates, lower hatching rates, and increased malformations in groups exposed to rhodamine B. Moreover, rhodamine B induced oxidative stress in F1 generation larvae, as evidenced by elevated levels of reactive oxygen species and altered antioxidant enzyme activity. Neurotoxicity assessments revealed reduced acetylcholinesterase activity, indicating potential neurological impairments in F1 generation larvae. Additionally, locomotory defects and skeletal abnormalities were observed in F1 generation larvae exposed to rhodamine B. This study provides comprehensive evidence of the reproductive toxicity of rhodamine B in adult zebrafish and its transgenerational effects on the F1 generation.

A comprehensive review on environmental pollutants and osteoporosis: Insights into molecular pathways.

A significant problem that has an impact on community wellbeing is environmental pollution. Environmental pollution due to air, water, or soil pollutants might pose a severe risk to global health, necessitating intense scientific effort. Osteoporosis is a common chronic condition with substantial clinical implications on mortality, morbidity, and quality of life. It is closely linked to bone fractures. Worldwide, osteoporosis affects around 200 million people, and every year, there are almost 9 million fractures. There is evidence that certain environmental factors may increase the risk of osteoporosis in addition to traditional risk factors. It is crucial to understand the molecular mechanisms at play because there is a connection between osteoporosis and exposure to environmental pollutants such as heavy metals, air pollutants, endocrine disruptors, metal ions and trace elements. Hence, in this scoping review, we explore potential explanations for the link between pollutants and bone deterioration through deep insights into molecular pathways. Understanding and recognizing these pollutants as modifiable risk factors for osteoporosis would possibly help to enhance environmental policy thereby aiding in the improvement of bone health and improving patient quality of life.