The impact of polar fraction of the fine particulate matter on redox responses in different rat tissues

Toxicological Effects of Fine Particulate Matter (PM2.5): Health Risks and Associated Systemic Injuries—Systematic Review

“…Renal redox imbalance was observed in rats exposed to PM 2.5 , as well as a significant decrease in glutamate-cysteine ligase activity and increased glutathione S-transferase activity. Changes observed in total antioxidant capacity (ACAP) in the cortex and renal medulla have shown that the models’ kidneys were sensitive to oxidative stress caused by exposure to PM 2.5 (de Paula et al, 2019 ). Morphological changes (glomerular atrophy, tubular damage), creatinine rise and caspase-3 expression were observed in animals exposed to PM 2.5 for six months (Hsu et al, 2019 ).…”

“…PM 2.5 presents heterogeneous composition, and its compounds can interact in different ways. Among the aforementioned compounds, metals emerge as an important pro-oxidative factor capable of increasing ROS formation (Fang et al, 2019 ; Ribeiro et al, 2016 ; de Paula et al, 2019 ). Although metallic ions are closely related to ROS formation, researchers attribute the oxidative condition to quinones, such as polycyclic aromatic hydrocarbons (PAHs) .…”

“…An assay performed in vitro by Xu et al, ( 2020 ) has evidenced that macrophage cells exposed to PM 2.5 solution (200 µg mL −1 ) for 6 h showed increased ROS levels and secretion of pro-inflammatory cytokines, such as IL-1β and TNF-α, which are associated with systemic inflammation. Reports have indicated that exposure to PM 2.5 decreased antioxidant defense in different organs, such as heart, kidney, liver and lung, by reducing antioxidants’ mechanism, and by affecting glutathione levels and total antioxidant capacity (Ribeiro et al, 2016 ; de Paula et al, 2019 ), as well as the activity of enzymes such as superoxide dismutase and glutathione peroxidase (Wu et al, 2016 ). Exposure to PM 2.5 plays a critical part in oxidative stress conditions, since it increases lipoperoxidation (Qiu et al, 2019 ; de Paula et al, 2019 ; Wang et al, 2019 ; Yu et al, 2017 ) and leads to mitochondrial damage (Guo et al, 2017 ; Jin et al, 2018 ; Wang et al, 2019 ).…”

“…Reports have indicated that exposure to PM 2.5 decreased antioxidant defense in different organs, such as heart, kidney, liver and lung, by reducing antioxidants’ mechanism, and by affecting glutathione levels and total antioxidant capacity (Ribeiro et al, 2016 ; de Paula et al, 2019 ), as well as the activity of enzymes such as superoxide dismutase and glutathione peroxidase (Wu et al, 2016 ). Exposure to PM 2.5 plays a critical part in oxidative stress conditions, since it increases lipoperoxidation (Qiu et al, 2019 ; de Paula et al, 2019 ; Wang et al, 2019 ; Yu et al, 2017 ) and leads to mitochondrial damage (Guo et al, 2017 ; Jin et al, 2018 ; Wang et al, 2019 ). Accordingly, mitochondrial injury opens the transition pore and hinders the potential of the mitochondrial membrane (Qiu et al, 2019 ; Wang et al, 2019 ).…”

“…Harmful effects of exposure to PM 2.5 and their association with damage in the human renal system were reported in different studies, which evidenced the risk of chronic kidney disease (CKD) (Blum et al, 2020 ; Bo et al, 2021 ; Bragg-Gresham et al, 2018 ; Chan et al, 2018 ), of progression to end-stage kidney disease—ESKD (Bowe et al, 2018 ) and of lower glomerular filtration rate (GFR) (Mehta et al, 2016 ). The aforementioned data indicate the scientific community’s growing interest in investigating the association between exposure to PM 2.5 and renal dysfunction (Mehta et al, 2016 ; de Paula et al, 2019 ; Xu et al, 2016 ). Concerning the gastrointestinal system, studies have also reported increased mortality rates associated with liver, colorectal, and gastrointestinal cancer, as well as with dysbiosis resulting from exposure to PM 2.5 (Liu et al, 2021 ; Pan et al, 2016 ; Weinmayr et al, 2018 ; Wong et al, 2016 ).…”