Hazardous effects of chemical pesticides on human health–Cancer and other associated disorders

Sabarwal, Akash; Kumar, Kunal; Singh, Rana P.

doi:10.1016/j.etap.2018.08.018

Cited by 457 publications

(244 citation statements)

References 144 publications

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“…In degeneration, alterations in native NP cell behavior occur in respect of proliferation, differentiation, dysregulated metabolism and cell death (Gruber & Hanley, 1998;Sabarwal, Kumar, & Singh, 2018).…”

mentioning

confidence: 99%

Retracted: Effects of IGFBP3 gene silencing mediated inhibition of ERK/MAPK signaling pathway on proliferation, apoptosis, autophagy, and cell senescence in rats nucleus pulposus cells

Chen

Zhou

2018

Journal Cellular Physiology

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Objective Disc degeneration is the common life‐threatening disease characterized by flank pain. The gene expression of insulin‐like growth factor binding protein 3 (IGFBP3) is increased in patients with disc degeneration, however, its mechanism is still unknown. This study aimed to investigate the influence of IGFBP3 gene silencing mediated inhibition of extracellular signal‐related kinase (ERK)/mitogen‐activated protein kinase (MAPK) signaling on proliferation, apoptosis, autophagy, and cell senescence in rats nucleus pulposus (NP) cells. Methods The expression of IGFBP3 in disc NP of patients was assessed by real‐time PCR (RT‐PCR) and western blot. RT‐PCR, transwell assay, immunohistochemical staining, SA‐β‐Gal staining, and western blot were performed to explore the molecular mechanism of IGFBP3 in NP cell migration and invasion. Results In this study, IGFBP3 was highly expressed in disc NP of patients. With RT‐PCR, transwell assay, immunohistochemical staining, SA‐β‐Gal staining, and western blot, downregulated IGFBP3 could inhibit NP cells' migration and invasion by targeting the ERK/MAPK signaling pathway. Conclusion Our findings revealed that the inhibition of the ERK/MAPK pathway was mediated by IGFBP3 silencing that had effects on proliferation, apoptosis, autophagy, and cell senescence. Furthermore, our findings suggested the underlying mechanism of disc degeneration.

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confidence: 99%

Retracted: Effects of IGFBP3 gene silencing mediated inhibition of ERK/MAPK signaling pathway on proliferation, apoptosis, autophagy, and cell senescence in rats nucleus pulposus cells

Chen

Zhou

2018

Journal Cellular Physiology

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“…Pesticides have been shown to lead to human cancer. For example, the pesticides that have alkyl ureas or amines are connected to brain tumors; dieldrin induces tumorigenesis of the lung, liver, lymphoid tissues, uterus, as well as thyroid; and the risk for prostate cancer is higher in patients exposed to Agent Orange . A prior investigation revealed that a trivalent pesticide‐related chemical can cause protein carbonylation and oxidative DNA damage in human urothelial cells, ultimately resulting in bladder cancer …”

Section: Discussionmentioning

confidence: 99%

Dysbiosis signatures of the microbial profile in tissue from bladder cancer

Liu

Lü

et al. 2019

Cancer Medicine

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BackgroundTo examine the microbial profiles in parenchyma tissues in bladder cancer.MethodsTissue samples of cancerous bladder mucosa were collected from patients diagnosed with bladder cancer (22 carcinoma tissues and 12 adjacent normal tissues). The V3‐V4 region of the bacterial 16S rRNA gene was PCR amplified, followed by sequencing on an Illumina MiSeq platform. Bioinformatics analysis for microbial classification and functional assessment was performed to assess bladder microbiome diversity and variations.ResultsThe predominant phylum in both tissues was Proteobacteria. The cancerous tissues exhibited lower species richness and diversity. Beta diversity significantly differed between the cancerous and normal tissues. Lower relative abundances of the microbial genera Lactobacillus, Prevotella_9, as well as Ruminococcaceae were observed, whereas those of Cupriavidus spp., an unknown genus of family Brucellaceae, and Acinetobacter, Anoxybacillus, Escherichia‐Shigella, Geobacillus, Pelomonas, Ralstonia, and Sphingomonas were higher in the cancerous tissues. These findings indicate that these genera may be potentially utilized as biomarkers for bladder cancer. PICRUSt analysis revealed that several pathways involved in the metabolism of harmful chemical compounds were enriched in the cancer tissues, thereby providing evidence that environmental factors are strongly associated with bladder cancer etiology.ConclusionThis is the first study that has described and analyzed the dysbiotic motifs of urinary microbiota in the parenchymatous tissues of bladder cancer via 16S rRNA gene sequencing. Our results suggest that changes in the bladder microbiome may serve as biomarkers for bladder cancer, possibly assisting in disease screening and monitoring.

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“…The antioxidant impacts were likewise examined if there should be an occurrence of Aβ‐infused rodents appearing neurotoxicity, with an accentuation on Nrf2/HO‐1 protection pathway (Gupta et al, ; Sabarwal, Kumar, & Singh, ; Tiwari et al, ). Nrf2, which is held with Kelch‐like erythroidcellderived protein 1 (Keap1) in the cytoplasm of the cell, is discharged from the complex under states of OS (additionally alluded to as electrophilic stress) and is enacted.…”

Section: Discussionmentioning

confidence: 99%

“…*** (p ≤ .001) versus Sham, + (p ≤ .05), ++ (p ≤ .01) and +++ (p ≤ .001) versus Aβ-infused group of rats. QCR, quercetin with an accentuation on Nrf2/HO-1 protection pathway Sabarwal, Kumar, & Singh, 2018;Tiwari et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Activation of Nrf2 signaling by sitagliptin and quercetin combination against β‐amyloid induced Alzheimer's disease in rats

Tian

et al. 2019

Drug Development Research

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The objective of this study was to evaluate the neuroprotective effect of sitagliptin (Sita), quercetin (QCR) and its combination in β‐amyloid (Aβ) induced Alzheimer's disease (AD). Male Sprague–Dawley rats, weighing between 220 and 280 g were used for experiment. Rats were divided into 5 groups (n = 10) and the groups were as follows: (a) Sham control; (b) Aβ injected; (c) Aβ injected + Sita 100; (d) Aβ injected + QCR 100; and (e) Aβ injected + Sita 100 + QCR 100. Cognitive performance was observed by the Morris water maze (MWM), biochemical markers, for example, MDA, SOD, CAT, GSH, Aβ1‐42 level, Nrf2/HO‐1 expression and histopathological study of rat brain were estimated. Pretreatment with Sita, QCR and their combination showed a significant increase in escape latency in particular MWM cognitive model. Further co‐administration of sita and QCR significantly reduced Aβ1‐42 level when compared with individual treatment. Biochemical markers, for example, increased SOD, CAT and GSH, decreased MDA were seen, and histopathological studies revealed the reversal of neuronal damage in the treatment group. Additionally, Nrf2/HO‐1 pathway in rat's brain was significantly increased by Sita, QCR and their combination. Pretreatment with QCR potentiates the action of Sita in Aβ induced AD in rats. The improved cognitive memory could be because of the synergistic effect of the drugs by decreasing Aβ1‐42 level, antioxidant activity and increased expression of Nrf2/HO‐1 in rat brain.

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Hazardous effects of chemical pesticides on human health–Cancer and other associated disorders

Cited by 457 publications

References 144 publications

Retracted: Effects of IGFBP3 gene silencing mediated inhibition of ERK/MAPK signaling pathway on proliferation, apoptosis, autophagy, and cell senescence in rats nucleus pulposus cells

Retracted: Effects of IGFBP3 gene silencing mediated inhibition of ERK/MAPK signaling pathway on proliferation, apoptosis, autophagy, and cell senescence in rats nucleus pulposus cells

Dysbiosis signatures of the microbial profile in tissue from bladder cancer

Activation of Nrf2 signaling by sitagliptin and quercetin combination against β‐amyloid induced Alzheimer's disease in rats

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