Biochimica et Biophysica Acta (BBA) - Bioenergetics
Mitochondrial bioenergetics as affected by DDT
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1,1,1-trichloro-2,2-bis (p-chlorophenyl)-ethane (DDT) and 1,1-Dichloro-2,2-bis (p, p’-chlorophenyl) ethylene (DDE) as endocrine disruptors in human and wildlife: A possible implication of mitochondria
2021, Environmental Toxicology and PharmacologyCitation Excerpt :DDT and DDE mitotoxicity was established 20–40 years ago, and Elmore and La Merrill (2019) recently reviewed their effect on mammalian mitochondrial oxidative phosphorylation, showing that both xenobiotics impaired ETC and oxidative phosphorylation. DDT and DDE elicited impairment in cellular respiration and mitochondrial membrane potential in mammalian mitochondria (Moreno and Madeira, 1991; Ohyama et al., 1982; Ferreira et al., 1997; Byczkowski, 1976). In vitro studies, mainly in rodent mitochondria, clearly demonstrated toxic effect of DDT and DDE on Complex II (succinate dehydrogenase) and Complex V (ATP synthase) of the ETC (Moreno and Madeira, 1991; Ohyama et al., 1982; Ferreira et al., 1997; Pardini et al., 1980).
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2020, Toxicology ReportsCitation Excerpt :This is consistent with the findings of Fleming et al. (1994), where p,p’-DDT, another DDT metabolite, was found to be significantly higher in AD brain samples [18]. DDT has also long been known to cause mitochondrial dysfunction [56], a process heavily involved in PD pathogenesis as well [57], and DDT and its derivatives have been shown to promote neuronal cell apoptosis by activating MAPKs (mitogen-activated protein kinases) [58]. Hexachlorobenzene exposure has been less studied compared to DDT and p,p’-DDE, probably pertaining to the fact that it was widely banned as a fungicide several decades ago and is nowadays solely used for laboratory purposes [59].
DDT exposure induces cell cycle arrest and apoptosis of skin fibroblasts from Indo-Pacific humpback dolphin via mitochondria dysfunction
2019, Aquatic ToxicologyCitation Excerpt :Mitochondrial dysfunction that causes cell death has been demonstrated in human cells exposed to DDT (Benachour et al., 2007). Previous investigations also showed that DDT inhibited mitochondrial ATP synthase (Van Tonder et al., 2014; Morena and Madeira, 1991; Younis et al., 2002). In this study, p,p’-DDT from 56 to 168 μM significantly depleted mitochondrial transmembrane potentials (ΔΨm) (p < 0.05, Fig. 5A), and significantly decreased ATP production (p < 0.05, Fig. 5B), indicating that p,p’-DDT could cause mitochondrial dysfunction.
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