Carbofuran accelerates the cellular senescence and declines the life span of <i>spns1</i> mutant zebrafish

Khan, Alam; Fahad, Talukdar Mohammad; Akther, Tanjima; Zaman, Tanjeena; Hasan, Faruk; Khan, Rafiqual Islam; Islam, Mohammad Saiful; Kishi, Shuji

doi:10.1111/jcmm.16171

Cited by 13 publications

(7 citation statements)

References 61 publications

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“…As has been previously shown, spns1 −/− mutant larvae show increased lysosomes by 3.5 dpf ( Figure 1 A,B) [ 12 , 25 , 26 ]. Although beta-galactosidase [ 16 ] has been observed in spns1 −/− muscle, the effects of lacking spns1 on muscle structure have not previously been reported.…”

Section: Resultssupporting

confidence: 74%

Lysosomal Function Impacts the Skeletal Muscle Extracellular Matrix

Coffey

Astumian

Alrowaished

et al. 2021

JDB

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Muscle development and homeostasis are critical for normal muscle function. A key aspect of muscle physiology during development, growth, and homeostasis is modulation of protein turnover, the balance between synthesis and degradation of muscle proteins. Protein degradation depends upon lysosomal pH, generated and maintained by proton pumps. Sphingolipid transporter 1 (spns1), a highly conserved gene encoding a putative late endosome/lysosome carbohydrate/H+ symporter, plays a pivotal role in maintaining optimal lysosomal pH and spns1−/− mutants undergo premature senescence. However, the impact of dysregulated lysosomal pH on muscle development and homeostasis is not well understood. We found that muscle development proceeds normally in spns1−/− mutants prior to the onset of muscle degeneration. Dysregulation of the extracellular matrix (ECM) at the myotendinous junction (MTJ) coincided with the onset of muscle degeneration in spns1−/− mutants. Expression of the ECM proteins laminin 111 and MMP-9 was upregulated. Upregulation of laminin 111 mitigated the severity of muscle degeneration, as inhibition of adhesion to laminin 111 exacerbated muscle degeneration in spns1−/− mutants. MMP-9 upregulation was induced by tnfsf12 signaling, but abrogation of MMP-9 did not impact muscle degeneration in spns1−/− mutants. Taken together, these data indicate that dysregulated lysosomal pH impacts expression of ECM proteins at the myotendinous junction.

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Section: Resultssupporting

confidence: 74%

Lysosomal Function Impacts the Skeletal Muscle Extracellular Matrix

Coffey

Astumian

Alrowaished

et al. 2021

JDB

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“…2,15 Recently, we reported that carbofuran hastens the developmental senescence in spns1-mutant zebrafish and affects their lifespan. 16 The current study extends the report in wild zebrafish, whereas we found carbofuran affects cellular autophagy and accelerates developmental senescence in both wild and spns1-mutant zebrafish.…”

Section: D B a E Fsupporting

confidence: 88%

“…In survival analysis, we reconfirmed that carbofuran exposure significantly shortened the lifespan of spns1 ‐mutant zebrafish (Figure 1E ). 16 Additionally, using a real‐time survival study, we found carbofuran significantly abated the survival lengths of wild zebrafish (Figure 1F ), suggesting carbofuran affects lifespan of both wild and spns1 −/− mutant fishes.…”

Section: Resultsmentioning

confidence: 85%

Carbofuran affects cellular autophagy and developmental senescence through the impairment of Nrf2 signalling

Khan

Zaman

Fahad

et al. 2021

J Cellular Molecular Medi

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Senescence is a cellular response towards various stresses, characterized by the permanent proliferative arrest on cells. 1 Pharmacological and/or genetic ablation of senescence/senescent cells improve health outcomes and extend the lifespan. 2 Autophagy is a lysosome-mediated cellular catabolic process, implicated with cellular senescence. In regulating the cellular homeostasis, autophagy usually suppresses cellular senescence by eliminating damaged cytoplasmic organelles and macromolecules. 3 In contrast, autophagy can also be activated by cellular senescence and up-regulated in senescent cells. 3 Under normal physiological conditions, cellular autophagy occurs at low baseline levels, which are up-regulated under various pathological conditions such as oxidative stress, starvation

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“…Higher carbofuran doses can also disrupt the metabolism of cells, including Purkinje cells. This disruption can interfere with the normal function of these cells and lead to cell death [17]. High carbofuran doses can damage cellular structures, including cell membranes and organelles.…”

Section: Resultsmentioning

confidence: 99%

The Influence of Carbofuran on Purkinje cells death in the fetal cerebellum of mice (Mus Musculus)

Rio Darlis Ahyari,

Maslichah Mafruchati,

Widjiati Widjiati

et al. 2024

Open Access Res. J. Biol. Pharm.

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The objective of this research was to assess the extent of damage to cerebellar Purkinje cells in fetal mice caused by exposure to the insecticide carbofuran during the embryonic period. The study involved eighteen pregnant female mice (Mus Musculus) exposed to carbofuran from gestational days 14 to 17. The female mice were divided into three groups: P0 (treated with physiological NaCl solution), P1 (treated with carbofuran at 0.0208 mg/Kg/day), and P2 (treated with carbofuran at 0.0417 mg/Kg/day). The data were analyzed using ANOVA and followed by the BNJ test. The results indicated a significant difference, with an increase in Purkinje cell necrosis corresponding to the dose of carbofuran.

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Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish

Cited by 13 publications

References 61 publications

Lysosomal Function Impacts the Skeletal Muscle Extracellular Matrix

Lysosomal Function Impacts the Skeletal Muscle Extracellular Matrix

Carbofuran affects cellular autophagy and developmental senescence through the impairment of Nrf2 signalling

The Influence of Carbofuran on Purkinje cells death in the fetal cerebellum of mice (Mus Musculus)

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