Mechanism underlying carbon tetrachloride-inhibited protein synthesis in liver

Figure 1 CCl₄ inhibits protein synthesis (A) and increases malondialdehyde production (B) in liver of Sprague-Dawley rats. Data are expressed as mean ± SE. ^aP < 0.05 vs control group; ^bP < 0.01 vs their counterpart control group; ^dP < 0.01 vs CCl₄ treatment group.

Figure 2 CC1₄ inhibits nucleotide triphosphatase affinity in nuclei of HepG2 cells. A: Methyl thiazolyl tetrazolium (MTT) metabolic viability assay at a dose of 10 mmol/L showing the inhibitory effect of CCl₄ on growth of HepG2 cells; B: Substrate-affinity (Km, B2) is decreased without any alterations in the substrate binding sites (Vmax,B1) for adenosine triphosphate (ATP) or guanine triphosphate (GTP) in nuclear nucleotide triphosphatase of HepG2 cells treated with CCl₄ (2 mmol/L); C: Enzyme’ activities of nuclei extracts and homogenates from HepG2 cells in control and CCl₄ treatment groups. ^aP < 0.05 vs control group, or nuclear envelop group, respectively; ^bP < 0.01 vs their counterpart control group, or nuclear envelop group, respectively. LDH: Lactose dehydrogenase.

Figure 3 Involvement of reactive radicals in decreased nucleotide triphosphatase activity of nuclei. Data are represented as mean ± SE. ^bP < 0.01 vs H₂O₂/Fe²⁺ group [(0 μmol/L)/(0 μmol/L)]. NTPase: Nucleotide triphosphatase.

Figure 4 CCl₄ decreases total mRNA nuclear export of HepG2 cells. DAPI: 4,6-diamidino-2-phenylindole dihydrochloride; FITC: Fluorescein isothiocyanate.