Salicylic acid triggers genotoxic adaptation to methyl mercuric chloride and ethyl methane sulfonate, but not to maleic hydrazide in root meristem cells of Allium cepa L.

Salicylic acid (SA), 0.01 mM, a signalling phytohormone, was tested for induction of adaptive response against genotoxicity of methyl mercuric chloride (MMCl), 0.013 mM; ethylmethane sulfonate (EMS), 2.5 mM, or maleic hydrazide (MH), 5 mM, in root meristem cells of Allium cepa. Induction of adaptive response to EMS by hydrogen peroxide (H2O2), 1 mM, and yet another secondary signal molecule was tested for comparison. Assessed by the incidence of mitoses with spindle and/or chromosome aberration and micronucleus, the findings provided evidence that SA-conditioning triggered adaptive response against the genotoxic-challenges of MMCl and EMS, but failed to do so against MH. H2O2, which is known to induce adaptive response to MMCl and MH, failed to induce the same against EMS in the present study. The findings pointed to the possible role of signal transduction in the SA-induced adaptive response to genotoxic stress that perhaps ruled out an involvement of H2O2.

Persistence and prevention of aluminium- and paraquat-induced adaptive response to methyl mercuric chloride in plant cells in vivo.

Induction and persistence of adaptive response by aluminium (Al), 1 or 10 microM, and paraquat (PQ), 5 or 10 microM, against genotoxicity of methyl mercuric chloride (MMCl), 1.26 microM, a standard environmental genotoxin, was investigated in root meristem cells of Allium cepa. Subsequently, three metabolic inhibitors, namely, 3-aminobezamide (3-AB, 10 or 100 microM), an inhibitor of poly(ADP-ribose) polymerase (PARP) implicated in DNA repair and/or apoptosis, cycloheximide (CH, 0.1 or 1 microM), an inhibitor of protein synthesis, and buthionine sulfoximine (BSO, 100 microM or 1mM), an inhibitor of glutathione synthesis were tested for their ability to prevent the adaptive response induced by conditioning doses of Al, 10 or 100 microM; and PQ, 5 or 100 microM, against MMCl-challenge, 1.26 or 100 microM, in root meristems of A. cepa or embryonic shoots of Hordeum vulgare, respectively. The findings demonstrated that once triggered, the Al- or PQ-adaptive response to MMCl could persist for at least 48h in root meristems of A. cepa. Furthermore, the adaptive response could effectively be prevented by 3-AB, to a lesser degree by CH, and the least by BSO, suggesting primarily the involvement of PARP and implicating DNA repair in the underlying mechanisms of adaptive response in plant cells in vivo.

Tolerance and co-tolerance of the grass Chloris barbata Sw. to mercury, cadmium and zinc.

Races of Chloris barbata Sw. from a mercury-contaminated site in the vicinity of a chloralkali plant and from a non-contaminated site were tested for their relative tolerance to mercury, cadmium and zinc. Pre-rooted tillers of each of the races were grown in calcium nitrate solution, Ca(NO3 )2 , 4H2 O, l gl-1 with or without HgCI2 (0.001, 0.01, 0.05, 0.1 and mgl-1 ), CdSO4 .8H2 O (0.05, 1.0, 2.5 and 5 mg l-1 and ZnSO4 7H2 O (1, 5, 10, 20 and 40 mg l-1 ) for a period of 5 d, Metal tolerance was evaluated by the effects of the metal on root elongation. Races from the contaminated site were found to be metal-tolerant, as indicated by higher tolerance indices (TIs) than races from the non-contaminated site. Mercury and cadmium at lower concentrations and zinc at all concentrations stimulated root growth in tolerant races, resulting in a TI of more than 100%. This indicated a requirement of the metal ion for better root growth. Compared to non-tolerant races, the tolerant races exhibited higher catalase, peroxidase and acid phosphatase activities as well as higher thiol levels. The over-all study thus indicated that races of C. barbata from the mercury-contaminated site were not only tolerant to mercury but also co-tolerant to cadmium and zinc. Biochemical studies provided evidence that the tolerant races were physiologically distinct from the intolerant races.