Abstract
This cytogenetic and pharmacological study attempts to clarify genotoxicity-enhancement-effect of dl-α-tocopherol (one form of vitamin E) in combination with the herbicide 1,1'-dimetyl-4,4'-bipyridium dichloride (paraquat, PQ) on cultured anuran leukocytes using the superoxide dismutase-mimic Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin (Mn(III)TMpyP), the hydrogen peroxide-scavenger catalase and the electron donor nicotinamide adenine dinucleotido phosphate (NADPH). PQ only was found to induce structural chromosomal damage in cultured anuran leukocytes in a dose-dependent manner. PQ plus NADPH, which served as positive control, enhanced the genotoxic effect of PQ. Dl-α-tocopherol only did not induce any structural chromosomal damage in the leukocytes. PQ plus dl-α-tocopherol, however, enhanced the genotoxic effect of PQ. PQ plus Mn(III)TMpyP, PQ plus catalase and PQ plus Mn(III)TMpyP plus catalse suppressed the genotoxic effect of PQ. Furthermore, PQ plus dl-α-tocopherol-enhanced chromosomal damage was also inhibited by Mn(III)TMpyP plus catalase. These results suggest that dl-α-tocopherol in combination with PQ functions as an electron donor to PQ.
Highlights
This cytogenetic and pharmacological study attempts to clarify genotoxicity-enhancement-effect of dl-α-tocopherol in combination with the herbicide 1,1’-dimetyl-4,4’-bipyridium dichloride on cultured anuran leukocytes using the superoxide dismutase-mimic Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin (Mn(III)TMpyP), the hydrogen peroxidescavenger catalase and the electron donor nicotinamide adenine dinucleotido phosphate (NADPH)
I failed to find the fragile sites of damaged chromosomes no. 1 and no. 2 in group 6 leukocytes, but chromosomal breaks occurred in short arm of no. 1 chromosome in the same group leukocytes are likely to be caused more than the others
The results show that PQ induces structural chromosomal damage
Summary
This cytogenetic and pharmacological study attempts to clarify genotoxicity-enhancement-effect of dl-α-tocopherol (one form of vitamin E) in combination with the herbicide 1,1’-dimetyl-4,4’-bipyridium dichloride (paraquat, PQ) on cultured anuran leukocytes using the superoxide dismutase-mimic Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin (Mn(III)TMpyP), the hydrogen peroxidescavenger catalase and the electron donor nicotinamide adenine dinucleotido phosphate (NADPH). PQ plus dl-α-tocopherol-enhanced chromosomal damage was inhibited by Mn(III)TMpyP plus catalase These results suggest that dl-α-tocopherol in combination with PQ functions as an electron donor to PQ. Dl-α-tocopherol (α-TH) antioxidant-defense-system functions in inhibiting unsaturated fatty acids (UFAs) autoxidation that is a free radical chain reaction Functional disruption in this defense system promotes accumulation of reactive oxygen species (ROS) involved in induction of chromosomal damage. Mn(III)TMpyP has dismutation-reaction property that is conversion of superoxide (O2Ϫ) into hydrogen peroxide (H2O2) (PASTERNACK et al 1981) This substance has suppressive effect on ischemia/ reperfusion-induced O2Ϫ generation leading to rat renal DNA damage (LIANG et al 2009).
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