Zahed Hossain | PubMed Health

PubMed2006

Decline in ascorbate peroxidase activity--a prerequisite factor for tepal senescence in gladiolus.

Flower senescence was studied in Gladiolus cv. "Snow Princess" over five arbitrarily divided developmental stages (stage 1, half bloom; stage 2, full bloom; stage 3, beginning of wilting; stage 4, 50% wilting; stage 5, complete wilting) in terms of changes in fresh weight, antioxidant enzymes (superoxide dismutase, SOD; ascorbate peroxidase, APX; glutathione reductase, GR) activities and membrane integrity. A significant decrease in tepal fresh weight was observed over the senescence period (after stage 2). Membrane integrity was studied by measuring lipid peroxidation [in terms of thiobarbituric acid reactive substances (TBARS) content] and membrane stability index (MSI) percentage. Maximum TBARS content was recorded in stage 4 (50% wilting). This increase in lipid peroxidation over the senescence period was in close association with high degree of membrane deterioration expressed as decrease in membrane stability index percentage. A significant decrease (two and half-fold) in MSI% in stage 5 (as compared to stage 1) indicates complete membrane deterioration. Progressive increase in endogenous H2O2 level was recorded over senescence period. Maximum H2O2 content (19.7+/-1.4 micromol g(-1) DW) was recorded at stage 5 (complete wilting). Three different patterns were observed in antioxidant enzymes behavior over the senescence period. APX activity was declined significantly as, the flower entered stage 3 (beginning of wilting) from full bloom condition (stage 2). Progressive and significant increase in SOD activity was measured as a function of time. Maximum SOD activity (24.2+/-0.8 U mg(-1) DW) was recorded in stage 5 (three-fold increase over stage 1). GR activity initially increased up to stage 4 (50% wilting) and declined significantly thereafter (approximately seven-fold). An increase in endogenous H2O2 level during senescence may be the result of a programmed down-regulation of APX enzyme activity, which seems to be the prerequisite factor for initiating senescence process in gladiolus tepal.

Antioxidants↗

PubMed2002

Studies on the interaction between Ag(+) and DNA.

The interaction between silver ion and DNA has been followed by submarine gel electrophoresis. When pBR322 plasmid DNA was allowed to interact with silver(I) acetate, it was found to contain Form I and Form II bands whose intensity remained unchanged as the concentration of Ag(+) was increased from 0 to 50 mM. However, the mobility of the bands decreased as the concentration of Ag(+) was increased, indicating the occurrence of increased covalent binding of the metal ion with DNA. When 1:1 mixtures of silver(I) acetate and ascorbate were allowed to interact with plasmid and genomic DNAs, it was found that the mixtures were much more damaging to plasmid as well as genomic DNAs than silver(I) acetate or ascorbate alone. In the case of pBR322 plasmid DNA, the mixture at 12.5 mM concentration was found to be more damaging than the mixtures at both higher and lower concentrations. The increased DNA damage is believed to be due to free radicals produced from the oxidation of ascorbate by molecular oxygen where the metal ion was playing a catalytic role.

Acetates↗

PubMed2002

Studies on the interaction between Cd(2+) ions and nucleobases and nucleotides.

Cadmium is a potent carcinogen in rodents and has recently been accepted by the International Agency for Research on Cancer as a category 1 (human) carcinogen, but the molecular mechanism of its action remains largely unclear. It has however been suggested that cadmium-induced carcinogenesis may involve either direct or indirect interaction of Cd(2+) with DNA. In this study it is found that when Cd(2+) is allowed to interact with adenine and guanine, there is a marked change in the high performance liquid chromatography (HPLC) retention time for adenine but not for guanine. Since Cd(2+) is believed to bind covalently to adenine and guanine, the changes in retention time but absence of any cadmium in the peak fraction point to the following: (i) lability of cadmium-nucleobase adducts, and (ii) introduction of some kind of chemical modification in adenine but not in guanine as a result of covalent binding. This result is different from that for Ni(2+) in which case a change in retention time was observed for guanine but not for adenine.

Adenine↗

PubMed2002

Studies on the interaction between Cd(2+) ions and DNA.

Cadmium is a potent carcinogen in rodents and has recently been accepted by the International Agency for Research on Cancer as a category 1 (human) carcinogen, but the molecular mechanism of its action remains largely unclear. It has however been suggested that cadmium-induced carcinogenesis may involve either direct or indirect interaction of Cd(2+) with DNA. Cd(2+) is believed to bind covalently with N7 centres of adenine and guanine. At low concentrations (< or =50 mM), Cd(2+) is found to react with plasmid DNA to produce a mixture of Form I and Form II bands whereas at higher concentrations (> or =100 mM), Cd(2+) causes extensive damage to DNA at a pH 5.8 solution of cadmium nitrate. Within the range 0-100 mM (when pH is adjusted to 7.4 by adding NaOH) an increase in concentration of Cd(2+) is found to cause a decrease in the gel mobility rate of plasmid and an increase in the intensity of the Form II band. When plasmid DNA is digested with BamH1, only the Form III band is observed both in the presence and absence of Cd(2+). However, the mobility of the band is found to decrease with the increase in the concentration of Cd(2+). When the enzyme Ssp1 which cuts plasmid DNA at the AT sites is used instead of BamH1, two bands are observed in the presence of cadmium as against one band in the absence of cadmium. These results suggest that Cd(2+) binds covalently with DNA (possibly at G, A and T centres) and can form intrastrand bifunctional AT adducts but not the GG adducts. It may also be that neither GG nor AT adducts are formed and yet Ssp1 digestion is prevented because of a structural modification introduced in adenine by its interaction with Cd(2+). In the presence of antioxidants such as cysteine, glutathione and ascorbate (especially cysteine and ascorbate), DNA damage is found to be greater than expected for the combined effects of the antioxidant and Cd(2+). The increased DNA damage is believed to be due to the formation of reactive oxygen species (ROS).

Animals↗