Heavy metal associated health hazards: An interplay of oxidative stress and signal transduction.

Arsenic poisoning is a global health problem. Chronic exposure to arsenic has been associated with the development of a wide range of diseases and health problems in humans. Arsenic exposure induces the generation of intracellular reactive oxygen species (ROS), which mediate multiple changes to cell behavior by altering signaling pathways and epigenetic modifications, or cause direct oxidative damage to molecules. Antioxidants with the potential to reduce ROS levels have been shown to ameliorate arsenic-induced lesions. However, emerging evidence suggests that constructive activation of antioxidative pathways and decreased ROS levels contribute to chronic arsenic toxicity in some cases. This review details the pathways involved in arsenic-induced redox imbalance, as well as current studies on prophylaxis and treatment strategies using antioxidants.

https://www.mdpi.com/2218-273X/10/2/240/pdf

The Role of Reactive Oxygen Species in Arsenic Toxicity.

A comparative review of microplastics and nanoplastics: Toxicity hazards on digestive, reproductive and nervous system

Chlorpyrifos induces the apoptosis and necroptosis of L8824 cells through the ROS/PTEN/PI3K/AKT axis

Targeting the miR-122/PKM2 autophagy axis relieves arsenic stress.

Zinc alleviates arsenism in common carp: Varied change profiles of cytokines and tight junction proteins among two intestinal segments.

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health. However, the toxicity of antibiotics on aquatic organisms, especially the effects on the detoxification system and immune system, has not been thoroughly studied. Lycopene (LYC) is a naturally occurring hydrocarbon carotenoid, which has received extensive attention as a potential antioxidant. The aim of this study was to investigate whether LYC alleviates exogenous toxicity in carp induced by sulfamethoxazole (SMZ) and the underlying molecular mechanisms. The grass carp were treated with SMZ (0.3 μg L-1) and/or LYC (10 mg per kg body weight) for 30 days. Indexes, such as hepatic function-related including histopathological changes and biochemical parameters, detoxification system-related including the cytochrome P450 enzyme system and antioxidant system, and immune system-related including inflammatory and apoptosis processes were detected. The results showed that SMZ stress leads to significant pathological damage of the liver and induction of oxidative stress. LYC coadministration recovered the cytochrome p450-1A1 homeostasis and decreased SMZ-induced accumulation of intracellular reactive oxygen species (ROS). Mechanistically, indicators in the innate immune system (such as toll like receptors (TLRs), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and IL-8) and the apoptosis pathway (p53, PUMA, B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax), and Caspase-9/3) disclosed adaptive activation under SMZ exposure; these anomalies returned to normal or close-to-normal levels after LYC coadministration. Therefore, LYC dietary supplement possesses liver protective function against exogenous toxic compounds like SMZ, making LYC a functional aquatic feed ingredient for aquiculture.

Lycopene alleviates sulfamethoxazole-induced hepatotoxicity in grass carp ( Ctenopharyngodon idellus) via suppression of oxidative stress, inflammation and apoptosis

Hepatoprotective effects of zinc (II) via cytochrome P-450/reactive oxygen species and canonical apoptosis pathways after arsenite waterborne exposure in common carp.

Hongxian Yu

Papers

Zinc alleviates arsenism in common carp: Varied change profiles of cytokines and tight junction proteins among two intestinal segments.

Lycopene alleviates sulfamethoxazole-induced hepatotoxicity in grass carp ( Ctenopharyngodon idellus) via suppression of oxidative stress, inflammation and apoptosis

Hepatoprotective effects of zinc (II) via cytochrome P-450/reactive oxygen species and canonical apoptosis pathways after arsenite waterborne exposure in common carp.