Mitochondrion: a sensitive target for Pb exposure

Abstract

Pb exposure is a worldwide environmental contamination issue which has been of concern to more and more people. Exposure to environmental Pb and its compounds through food and respiratory routes causes toxic damage to the digestive, respiratory, cardiovascular and nervous systems, etc. Children and pregnant women are particularly vulnerable to Pb. Pb exposure significantly destroys children's learning ability, intelligence and perception ability. Mitochondria are involved in various life processes of eukaryotes and are one of the most sensitive organelles to various injuries. There is no doubt that Pb-induced mitochondrial damage can widely affect various physiological processes and cause great harm. In this review, we summarized the toxic effects of Pb on mitochondria which led to various pathological processes. Pb induces mitochondrial dysfunction leading to the increased level of oxidative stress. In addition, Pb leads to cell apoptosis via mitochondrial permeability transition pore (MPTP) opening. Also, Pb can stimulate the development of mitochondria-mediated inflammatory responses. Furthermore, Pb triggers the germination of autophagy via the mitochondrial pathway and induces mitochondrial dysfunction, disturbing intracellular calcium homeostasis. In a word, we discussed the effects of Pb exposure on mitochondria, hoping to provide some references for further research and better therapeutic options for Pb exposure.

Glycine protects the male reproductive system against lead toxicity via alleviating oxidative stress, preventing sperm mitochondrial impairment, improving kinematics of sperm, and blunting the downregulation of enzymes involved in the steroidogenesis

“…The adverse effects of Pb on cellular mitochondria is a critical mechanism of cytotoxicity induced by this heavy metal in various organs. 30,31 Pb could induce mitochondrial depolarization, ATP depletion, mitochondrial permeabilization, and release of cell death mediators form this organelle. 30,31 The current study showed a significant decrease in sperm ATP, mitochondrial depolarization, and mitochondrial dehydrogenases activity of Pb-exposed mice (Figure 6).…”

“…Thus, enhancing the sperm mitochondrial function is a strategy to improve its functionality indices. The adverse effects of Pb on cellular mitochondria is a critical mechanism of cytotoxicity induced by this heavy metal in various organs 30,31 . Pb could induce mitochondrial depolarization, ATP depletion, mitochondrial permeabilization, and release of cell death mediators form this organelle 30,31 .…”

“…27,28 It is well known that Pb could robustly induce mitochondrial permeabilization, depolarize the mitochondrial membrane, inhibit enzymes involved in energy metabolism, and finally, organ injury. [29][30][31] On the other hand, mitochondria play a central role in steroidogenesis. 32,33 Several enzymes involved in the steroidogenesis process are located in the mitochondrial membrane.…”

“…Mitochondria are vital organelles in male reproductive cells (e.g., Leydig cells) 27,28 . It is well known that Pb could robustly induce mitochondrial permeabilization, depolarize the mitochondrial membrane, inhibit enzymes involved in energy metabolism, and finally, organ injury 29–31 . On the other hand, mitochondria play a central role in steroidogenesis 32,33 .…”

Lead Disrupts Mitochondrial Morphology and Function through Induction of ER Stress in Model of Neurotoxicity

“…In our previous research, it was found that Pb exposure results in endoplasmic reticulum stress. Meanwhile, Pb exposure has also been shown to cause mitochondrial dysfunction [ 16 ]. Therefore, whether lead-induced ER stress is closely related to mitochondrial dysfunction is worthy of further study.…”