TY - JOUR
T1 - Role of Nrf2 in bisphenol effects
T2 - a review study
AU - Salehabadi, Amin
AU - Farkhondeh, Tahereh
AU - Harifi-Mood, Mohammad Sadra
AU - Aschner, Michael
AU - Samarghandian, Saeed
N1 - Publisher Copyright:
© 2022, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
PY - 2022/8
Y1 - 2022/8
N2 - Bisphenols (BPs), the main endocrine-disrupting chemicals used in polycarbonate plastics, epoxy-phenol resins, and some other manufacturers, have been interestingly focused to find their toxic effects in recent years. Due to the strong relation between bisphenols and some crucial receptors such as ERs, AR, glucocorticoid receptor, THRs, ERRs, hPXR, AhR, and etcetera, the disrupting and oncogenic role of these chemicals on reproductive, respiratory, and circulatory systems and a broad group of body tissues have been investigated. BPs induce oxidant enzymes, exert antioxidant enzymes from body cells, and result in the expression of proinflammatory genes, leading to cell apoptosis and inflammation. To maintain the homeostasis of human body cells, Nrf2, the key regulator of oxidative stress (Ashrafizadeh et al., 2020a; Ashrafizadeh et al., 2020c; Boroumand et al., 2018), confronts BP-induced ROS and RNS through the activation of antioxidant enzymes such as SOD1/2, CAT, GSH, GPX, HO-1, and etcetera. Chemicals and drugs such as LUT, NAC, GEN, l-NMMA, Ph2Se2, and GE can regulate the interactions between BPs and Nrf2. Despite the vital role of controlled levels of Nrf2 as an anti-inflammatory and antiapoptotic element, the uncontrolled activity of this transcription factor could lead to cell proliferation and tumorigenesis through NQO1, SLC7a11, Gclm, HMOX1, NQO1 gene activation, and some other genes. To avoid the excessive activity of Nrf2, some protein complexes like CUL3-RBX1-Keap1 (as the primary regulator), β-TrCP, and WDR23 regulate Nrf2’s function. It is necessary to note that BPA, as the most famous member, is further reviewed due to its resemblance to the bisphenol family to each other.
AB - Bisphenols (BPs), the main endocrine-disrupting chemicals used in polycarbonate plastics, epoxy-phenol resins, and some other manufacturers, have been interestingly focused to find their toxic effects in recent years. Due to the strong relation between bisphenols and some crucial receptors such as ERs, AR, glucocorticoid receptor, THRs, ERRs, hPXR, AhR, and etcetera, the disrupting and oncogenic role of these chemicals on reproductive, respiratory, and circulatory systems and a broad group of body tissues have been investigated. BPs induce oxidant enzymes, exert antioxidant enzymes from body cells, and result in the expression of proinflammatory genes, leading to cell apoptosis and inflammation. To maintain the homeostasis of human body cells, Nrf2, the key regulator of oxidative stress (Ashrafizadeh et al., 2020a; Ashrafizadeh et al., 2020c; Boroumand et al., 2018), confronts BP-induced ROS and RNS through the activation of antioxidant enzymes such as SOD1/2, CAT, GSH, GPX, HO-1, and etcetera. Chemicals and drugs such as LUT, NAC, GEN, l-NMMA, Ph2Se2, and GE can regulate the interactions between BPs and Nrf2. Despite the vital role of controlled levels of Nrf2 as an anti-inflammatory and antiapoptotic element, the uncontrolled activity of this transcription factor could lead to cell proliferation and tumorigenesis through NQO1, SLC7a11, Gclm, HMOX1, NQO1 gene activation, and some other genes. To avoid the excessive activity of Nrf2, some protein complexes like CUL3-RBX1-Keap1 (as the primary regulator), β-TrCP, and WDR23 regulate Nrf2’s function. It is necessary to note that BPA, as the most famous member, is further reviewed due to its resemblance to the bisphenol family to each other.
KW - Bisphenol A
KW - Bisphenols
KW - Nrf2
KW - Nuclear factor erythroid 2-related factor 2
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U2 - 10.1007/s11356-022-20996-3
DO - 10.1007/s11356-022-20996-3
M3 - Review article
C2 - 35680748
AN - SCOPUS:85131572677
SN - 0944-1344
VL - 29
SP - 55457
EP - 55472
JO - Environmental Science and Pollution Research
JF - Environmental Science and Pollution Research
IS - 37
ER -