Altered ontogeny of glutathione S-transferases by 2,4,5-2′,4′,5′-hexachlorobiphenyl

Lamartiniere, Coral A.; Dieringer, C.S.; Lucier, George W.

doi:10.1016/0041-008x(79)90465-4

Cited by 12 publications

(3 citation statements)

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“…Functional analysis of the list of DEG in IPA identified nuclear receptors (AHR, PXR, CAR, RXR, PPARGC-1α, NRF2, HNF4α) that are upstream regulators of pathways predicting induction of oxidative stress, xenobiotic/drug, hormone (thyroid, steroids), and lipid metabolisms. The IPA prediction of induction of oxidative stress is in agreement with studies observing elevated hepatic glutathione S-transferase (GST) activities in Sprague-Dawley rats exposed to TCDD (Baars, Jansen, and Breimer 1978) or to non-ortho or ortho-chlorinated PCB (Lamartiniere, Dieringer, and Lucier 1979;Twaroski, O'Brien, and Robertson 2001), which are present in the mixture. The current rats exhibited increased activities of the major liver enzymes involved in xenobiotic metabolism, including CYP1A, 2B, and 3A (Desaulniers et al 2017).…”

Section: Influence Of Developmental Exposure To Mixture M At Pnd21supporting

confidence: 83%

Effects of cross-fostering and developmental exposure to mixtures of environmental contaminants on hepatic gene expression in prepubertal 21 days old and adult male Sprague-Dawley rats

Desaulniers

Khan

Cummings-Lorbetskie

et al. 2019

Journal of Toxicology and Environmental Health, Part A

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Section: Influence Of Developmental Exposure To Mixture M At Pnd21supporting

confidence: 83%

Effects of cross-fostering and developmental exposure to mixtures of environmental contaminants on hepatic gene expression in prepubertal 21 days old and adult male Sprague-Dawley rats

Desaulniers

Khan

Cummings-Lorbetskie

et al. 2019

Journal of Toxicology and Environmental Health, Part A

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“…29,30,38,73,74 Fadhel et al 38 and Lamartinier et al 73 observed a significant increase in glutathione- S -transferase (GST) in Sprague–Dawley rats that were exposed to 150 μ mol/kg PCB 153 for six days and an increase in hepatic lipid peroxidation with a single dose of PCB 153. Twaroski et al 30 also reported similar findings from rats that received intraperitoneal injections of PCB 153 (100 mmol/kg for 3 wks).…”

Section: Resultsmentioning

confidence: 99%

Polychlorinated Biphenyls Induce Oxidative DNA Adducts in Female Sprague–Dawley Rats

Mutlu

Gao

Collins

et al. 2016

Chem. Res. Toxicol.

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Polychlorinated biphenyls (PCBs) are organic chemicals that were traditionally produced and widely used in industry as mixtures and are presently formed as byproducts of pigment and dye manufacturing. They are known to persist and bioaccumulate in the environment. Some have been shown to induce liver cancer in rodents. Although the mechanism of the toxicity of PCBs is unknown, it has been shown that they increase oxidative stress, including lipid peroxidation. We hypothesized that oxidative stress-induced DNA damage could be a contributor for PCB carcinogenesis and analyzed several DNA adducts in female Sprague–Dawley rats exposed to 3,3′,4,4′,5-pentachlorobiphenyl (PCB 126), 2,2′,4,4′,5,5′-hexachlorobiphenyl (PCB 153), and a binary mixture (PCB 126 + 153) for 14, 31, and 53 wks. Eight adducts were measured to profile oxidative DNA lesions, including 8-oxo-deoxyguanosine (8-oxo-dG), 1,N6-ethenodeoxyadenosine (1,N6-εdA), N2,3-ethenoguanine (N2,3-εG), 1,N2-ethenodeoxyguanosine (1,N2-εdG), as well as malondialdehyde (M1dG), acrolein (AcrdG), crotonaldehyde (CrdG), and 4-hydroxynonenal-derived dG adducts (HNEdG) by LC–MS/MS analysis. Statistically significant increases were observed for 8-oxo-dG and 1,N6-εdA concentrations in hepatic DNA of female rats exposed to the binary mixture (1000 ng/kg/day + 1000 μg/kg/day) but not in rats exposed to PCB 126 (1000 ng/kg/day) or PCB 153 (1000 μg/kg/day) for 14 and 31 wks. However, exposure to PCB 126 (1000 ng/kg/day) for 53 wks significantly increased 8-oxo-dG, 1,N6-εdA, AcrdG, and M1dG. Exposure to PCB 153 (1000 μg/kg/day) for 53 wks increased 8-oxo-dG, and 1,N6-εdA. Exposure to the binary mixture for 53 wks increased 8-oxo-dG, 1,N6-εdA, AcrdG, 1,N2-εdG, and N2,3-εG significantly above control groups. Increased hepatic oxidative DNA adducts following exposure to PCB 126, PCB 153, or the binary mixture shows that an increase in DNA damage may play an important role in hepatic toxicity and carcinogenesis in female Sprague–Dawley rats.

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“…These enzymes bind a large number of hydrophobic compounds and act as a storage facility before metabolism or excretion of the ligand (Jakoby & Keen, 1977) and undergo covalent-bond formation with reactive electrophilic carbon atoms (Keen & Jakoby, 1978). Some attention has been devoted to the postnatal developmental course of glutathione S-transferase (Hales & Neims, 1976a,b) and to its induction by xenobiotics (Darby & Grundy, 1972;Hales & Neims, 1977;Lamartiniere et al, 1979a), but little to its regulation by endocrine factors (Reyes et al, 1971). We have therefore initiated an in-depth study on the role that the hypothalamic-hypophyseal-gonadal axis plays in the sexual differentiation and regulation of hepatic glutathione S-transferases in the rat.…”

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confidence: 99%

The hypothalamic–hypophyseal–gonadal regulation of hepatic glutathione S-transferases in the rat

Lamartiniere

1981

Biochemical Journal

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Hepatic glutathione S-transferase activities were determined with the substrates 1,2-dichloro-4-nitrobenzene and 1-chloro-2,4-dinitrobenzene. Sexual differentiation of glutathione S-transferase activities is not evident during the prepubertal period, but glutathione conjugation with 1,2-dichloro-4-nitrobenzene is 2-3-fold greater in adult males than in females. Glutathione conjugation with 1-chloro-2,4-dinitrobenzene is slightly higher in adult males than adult females. No change in activity was observed after postpubertal gonadectomy of males or females. Neonatal castration of males results in a significant decrease in glutathione conjugation with 1,2-dichloro-4-nitrobenzene. Hypophysectomy, or hypophysectomy followed by gonadectomy did result in significantly higher glutathione S-transferase activities in both sexes. These increases can be reversed by implanting an adult male or female pituitary or four prepubertal pituitaries under the kidney capsule. Postpubertal sexual differentiation of glutathione S-transferase activities is neither dependent on pituitary sexual differentiation nor pituitary maturation. Prolactin concentrations are inversely related to glutathione S-transferase activities in hypophysectomized rats with or without ectopic pituitaries. Somatotropin exogenously administered to hypophysectomized rats results in decreased glutathione S-transferase activities, whereas prolactin has no effect. Adult male rats treated neonatally with monosodium l-glutamate to induce arcuate nucleus lesions of the hypothalamus have decreased glutathione S-transferase activities towards 1,2-dichloro-4-nitrobenzene and decreased somatotropin concentrations. Our experiments suggests that sexual differentiation of hepatic glutathione S-transferase is a result of a hypothalamic inhibiting factor in the male (absent in the female). This postpubertally expressed inhibiting factor acts on the pituitary to prevent secretion of a pituitary inhibiting factor (autonomously secreted by the female), resulting in higher glutathione S-transferase activities in the adult male than the adult female.

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Altered ontogeny of glutathione S-transferases by 2,4,5-2′,4′,5′-hexachlorobiphenyl

Cited by 12 publications

References 12 publications

Effects of cross-fostering and developmental exposure to mixtures of environmental contaminants on hepatic gene expression in prepubertal 21 days old and adult male Sprague-Dawley rats

Effects of cross-fostering and developmental exposure to mixtures of environmental contaminants on hepatic gene expression in prepubertal 21 days old and adult male Sprague-Dawley rats

Polychlorinated Biphenyls Induce Oxidative DNA Adducts in Female Sprague–Dawley Rats

The hypothalamic–hypophyseal–gonadal regulation of hepatic glutathione S-transferases in the rat

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