No abstract

No abstract

Objectives Oxidative stress is the most common factor mediating environmental chemical-induced health adversities. Recently, an exponential rise in the use of phytochemicals as an alternative therapeutics against oxidative stress-mediated diseases has been documented. Due to their free radical quenching property, plant-derived natural products have gained substantial attention as a therapeutic agent in environmental toxicology. The present review aimed to describe the therapeutic role of phytochemicals in mitigating environmental toxicant-mediated sub-cellular and organ toxicities via controlling cellular antioxidant response. Methods The present review has covered the recently related studies, mainly focussing on the free radical scavenging role of phytochemicals in environmental toxicology. Key findings In vitro and in vivo studies have reported that supplementation of antioxidant-rich compounds can ameliorate the toxicant-induced oxidative stress, thereby improving the health conditions. Improving the cellular antioxidant pool has been considered as a mode of action of phytochemicals. However, the other cellular targets of phytochemicals remain uncertain. Conclusions Knowing the therapeutic value of phytochemicals to mitigate the chemical-induced toxicity is an initial stage; mechanistic understanding needs to decipher for development as therapeutics. Moreover, examining the efficacy of phytochemicals against mixer toxicity and identifying the bioactive molecule are major challenges in the field.

Benzene, a ubiquitous environmental chemical, is known to cause immune dysfunction and developmental defects. This study aims to investigate the relation between benzene-induced immune dysfunction and developmental toxicity in a genetically tractable animal model, Drosophila melanogaster. Further, the study explored the protective role of Heat Shock Protein 70 (Hsp70) against benzene-induced immunotoxicity and subsequent developmental impact. Drosophila larvae exposed to benzene (1.0, 10.0, and 100.0 mM) were examined for total hemocyte (immune cells) count, phagocytic activity, oxidative stress, apoptosis, and their developmental delay and reduction were analyzed.Benzene exposure for 48 h reduced the total hemocytes count and phagocytic activity, along with an increase in the Reactive Oxygen Species (ROS), and lipid peroxidation in the larval hemocytes. Subsequently, JNK-dependent activation of the apoptosis (Caspase-3 dependent) was also observed. During their development, benzene exposure to Drosophila larvae led to 3 days of delay in development, and ~40% reduced adult emergence. Hsp70-overexpression in hemocytes was found to mitigate benzene-induced oxidative stress and abrogated the JNK-mediated apoptosis in hemocytes, thus restoring total hemocyte count and improving phagocytotic activity. Further, hsp70-overexpression in hemocytes also lessened the benzene-induced developmental delay (rescue of 2.5 days) and improved adult emergence (~20%) emergence, revealing a possible control of immune cells on the organism's development and survival. Overall, this study established that hsp70-overexpression in the Drosophila hemocytes confers protection against benzene-induced immune injury via regulating the ROS/JNK signaling pathway, which helps in the organism's survival and development.

No abstract