Acute Toxicity of Heavy Metals to Tetrahymena in an In Vitro Experiment and Envelope Damage Study

The toxicity of Cr3+, Cu2+ and Cd2+ to Tetrahymena growth metabolism was studied by microcalorimetry at 28A degrees C, and the growth constant (k), peak time (T) and generation times (T (G)) were calculated. The metal ion concentrations that resulted in 50 % inhibition (IC (50)) of population growth were obtained through the dynamic parameters. The results indicated that the order of toxicity was Cd2+ > Cr3+ > Cu2+. Inductively coupled plasma-atomic emission spectrometry results suggested that the metal ions affected the permeability of the cell membrane. Observations of the Cd-exposed organisms by scanning electron microscopy revealed damage to the cell membrane in the form of an altered surface appearance. The cells suffered serious damage after sufficient acting time. Attenuated total reflection Fourier transform infrared spectra revealed that amide groups and PO2 (-) of the phospholipid phospho-diester, both located in the hydrophobic end of the outer layer of the cell membrane, were most readily affected.The toxicity of Cr3+, Cu2+ and Cd2+ to Tetrahymena growth metabolism was studied by microcalorimetry at 28A degrees C, and the growth constant (k), peak time (T) and generation times (T (G)) were calculated. The metal ion concentrations that resulted in 50 % inhibition (IC (50)) of population growth were obtained through the dynamic parameters. The results indicated that the order of toxicity was Cd2+ > Cr3+ > Cu2+. Inductively coupled plasma-atomic emission spectrometry results suggested that the metal ions affected the permeability of the cell membrane. Observations of the Cd-exposed organisms by scanning electron microscopy revealed damage to the cell membrane in the form of an altered surface appearance. The cells suffered serious damage after sufficient acting time. Attenuated total reflection Fourier transform infrared spectra revealed that amide groups and PO2 (-) of the phospholipid phospho-diester, both located in the hydrophobic end of the outer layer of the cell membrane, were most readily affected