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FIGURE 1 Carbofuran exacerbates cellular senescence and shortens lifespan. (A) Based on the magnitude of opaqueness, the yolk opaqueness was sorted as partially opaque (marked by yellow colour) and mostly opaque (marked by red colour). Fish (wild type; spns1+/+ or heterozygote; spns1±) did not show opaqueness phenotype was marked by black colour. (B) The effect of carbofuran exposure on senescence phenotype (yolk opacity) of spns1-mutant zebrafish. In the cases of carbofuran-treated spns1-mutant zebrafish, both partially and mostly opaque phenotypes were found at earlier times than mutant zebrafish of the control group (egg water treatment). In addition, carbofuran treatment leads mutant zebrafish to die at quicker times than fish of the control group. (C) Survival (in hours) of spns1-mutant embryos has been shortened (P = .0003) upon exposure to carbofuran. (D) Survival (in months) of wild zebrafish was shortened (P < .0007) upon exposure to carbofuran. (E) Carbofuran accelerates SA-β-gal activity in both wild-type (spns1+/+) and spns1-mutant (spns1−/−) zebrafish. Carbofuran did not affect morphological phenotype (MP) of wild fish but affected yolk opaqueness of spns1-mutant fish (black arrowhead in the first row). SA-β-gal–stained fish have shown in the second row. The cellular SA-β-gal staining at dorsal to the eye has shown in the third row. (F) Quantification of dark blue particles of SA-β-gal staining of whole fish. The scale bar is 250 μm (stereo microscopic images) and 10 μm (confocal microscopic images). The number of fish was 10 (n = 10). Data are presented as mean ± SE. *P ≤ .05; ***P ≤ .005