Lipid Peroxidation and Changes of Trace Elements in Mice Treated with Paradichlorobenzene

Wang, Suhua; Lu, Rongzhu; Yin, Changlong; Xing, Guangwei; Han, Fei; Jing, Junjie; Xu, Wenrong; Aschner, Michael

doi:10.1007/s12011-009-8552-1

Cited by 8 publications

(4 citation statements)

References 59 publications

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“…This compound has central nervous system toxicity, causing oxidative damage and trace element alterations in various tissues, as well as oxidative DNA damage, leading to reported cognitive decline. 84,86,87 From our correlation network analysis showing several pathways between chemical biomarkers and cognitive decline, we observed that stroke had relatively strong correlation coefficients with both blood Cd and cognitive decline. This finding highlights the need of this network analysis because blood Cd had protective effects against cognitive decline when considering other identified environmental chemicals in the regression.…”

Section: Discussionmentioning

confidence: 84%

Environment-Wide Association Study of Cognitive Function in U.S. Older Adults using the NHANES Data

Jang,

Lee,

Nguyen

et al. 2024

Preprint

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Neurodegenerative diseases pose increasing challenges to global aging populations. Cognitive decline in older adults is an initial indicator of neurodegenerative diseases, yet comprehensive research on environmental chemical exposures related to cognitive decline is limited. This study uses Environment-Wide Association Study (EWAS) framework to investigate associations of environmental chemicals with cognitive function in individuals aged ≥60 years. We used the Digit Symbol Substitution Test (DSST) scores (lower scores indicate cognitive decline) and chemical biomarker data of the U.S. National Health and Nutrition Examination Survey (NHANES) spanning four cycles (1999-2000, 2001-2002, 2011-2012, 2013-2014). We conducted multiple survey-weighted regression to identify biomarkers associated with DSST scores, penalized logit regression to estimate odds ratio (OR) of cognitive decline with identified biomarkers, and correlation network analyses to examine relationships among identified biomarkers and cognitive decline. After correction for multiple comparisons, 27 out of 173 biomarkers having a ≥10% detection rate were associated with DSST scores (q-value <0.05). Among them, increased odds of cognitive decline were associated with elevated levels of blood lead (Pb) (OR = 1.12, 95% CI: 1.01,1.42), blood 1,4-dichlorobenzene (1,4-DCB) (OR = 1.34, 95% CI: 1.17, 1.54), and urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) (OR = 1.34, 95% CI: 1.10, 1.62). Correlation network showed biomarkers that potentially impact cognitive decline upon related health conditions, such as stroke. In conclusion, leveraging the EWAS framework enables us to identify chemical biomarkers that were not previously discovered from traditional approaches of examining a small number of chemicals at a time. While our findings provide foundation for further research, longitudinal studies are warranted to elucidate causal relationships.

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Section: Discussionmentioning

confidence: 84%

Environment-Wide Association Study of Cognitive Function in U.S. Older Adults using the NHANES Data

Jang,

Lee,

Nguyen

et al. 2024

Preprint

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“…A carcinogenic mechanism involving metabolism to hydroquinones has therefore been proposed. However, the ability of DCB to induce oxidative stress in vivo has been unclear ( Suhua et al. , 2010 ).…”

Section: Discussionmentioning

confidence: 99%

Evidence That the Capacity of Nongenotoxic Carcinogens to Induce Oxidative Stress Is Subject to Marked Variability

et al. 2015

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Many drugs and environmental chemicals which are not directly mutagenic have the capacity to increase the incidence of tumors in the liver and other tissues. For this reason, such compounds are known as nongenotoxic carcinogens. The mechanisms underlying their effects remain unclear; however, their capacity to induce oxidative stress is considered to be a critical step in the carcinogenic process, although the evidence that this is actually the case remains equivocal and sparse. We have exploited a novel heme oxygenase-1 reporter mouse to evaluate the capacity of nongenotoxic carcinogens with different mechanisms of action to induce oxidative stress in the liver in vivo. When these compounds were administered at doses reported to cause liver tumors, marked differences in activation of the reporter were observed. 1,4-Dichlorobenzene and nafenopin were strong inducers of oxidative stress, whereas phenobarbital, piperonyl butoxide, cyproterone acetate, and WY14,643 were, at best, only very weak inducers. In the case of phenobarbital and thioacetamide, the number of LacZ-positive hepatocytes increased with time, and for the latter also with dose. The data obtained demonstrate that although some nongenotoxic carcinogens can induce oxidative stress, it is not a dominant feature of the response to these compounds. Therefore in contrast to the current models, these data suggest that oxidative stress is not a key determinant in the mechanism of nongenotoxic carcinogenesis but may contribute to the effects in a compound-specific manner.

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“…In another study following inhalation exposure to PDCB for 10 days, researchers found that the concentration of the chemical compound peaked on day 6. The greatest concentration was found to be in adipose tissue, indicating the lipophilic nature of PDCB [Suhua et al 2010]. Oral administration of PDCB in Fischer 344 rats for 28 days showed that the blood plasma concentration peaked on the third day.…”

Section: Pharmacokinetics Of Pdcbmentioning

confidence: 99%

“…Alteration in levels of zinc, selenium and iron were also noted [Weintraub et al 2000]. This study suggested oxidative damage and alteration of trace elements in different tissues as the cause of toxicity [Suhua et al 2010]. Another study showed that some metabolites of PDCB – 2,5-DCHQ and 2,5-dichloro- p -benzoquinone (DCBQ) – can cause oxidative DNA damage in the presence of Cu( II ) and nicotinamide adenine dinucleotide (NADH) [Oikawa and Kawanishi, 1996].…”

Section: Mode Of Pdcb Toxicitymentioning

confidence: 99%

Para-dichlorobenzene toxicity – a review of potential neurotoxic manifestations

Dubey

Sharma

Pass

et al. 2014

Ther Adv Neurol Disord

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Lipid Peroxidation and Changes of Trace Elements in Mice Treated with Paradichlorobenzene

Cited by 8 publications

References 59 publications

Environment-Wide Association Study of Cognitive Function in U.S. Older Adults using the NHANES Data

Environment-Wide Association Study of Cognitive Function in U.S. Older Adults using the NHANES Data

Evidence That the Capacity of Nongenotoxic Carcinogens to Induce Oxidative Stress Is Subject to Marked Variability

Para-dichlorobenzene toxicity – a review of potential neurotoxic manifestations

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