DNA fragmentation, chromosomal aberrations, and multi-toxic effects induced by nickel and the modulation of Ni-induced damage by pomegranate seed extract in Allium cepa L

This study was designed to assess the recovery effect of pomegranate seed extract (PSEx) against nickel (Ni)-induced damage in Allium cepa. Except for the control group treated with tap water, five experimental groups were exposed to 265 mg L−1 PSEx, 530 mg L−1 PSEx, 1 mg L−1 NiCI2, 265 mg L−1 PSEx + 1 mg L−1 NiCI2, and 530 mg L−1 PSEx + 1 mg L−1 NiCI2, respectively. The toxicity of Ni was examined through the analysis of physiological (germination percentage, weight gain, and root length), cytotoxicity (mitotic index), genotoxicity (micronucleus, chromosomal anomalies, and Comet test), and biochemical (malondialdehyde, proline, chlorophyll a and chlorophyll b contents, the activities of superoxide dismutase and catalase) parameters. Meristematic cell defects were also investigated. The NiCl2-DNA interaction was evaluated through spectral shift analysis. Values of all physiological parameters, mitotic index scores, and chlorophyll contents decreased while micronucleus frequency, DNA tail percentage, chromosomal anomalies, proline, MDA, and enzyme activities increased following Ni administration. According to the tail DNA percentage scale, Ni application caused “high damage” to DNA. Ni-induced chromosomal anomalies were fragment, sticky chromosome, vagrant chromosome, bridge, unbalanced chromatin distribution, reverse polarization, and nucleus with bud. NiCl2-DNA interaction caused a hyperchromic shift in the UV/Vis spectrum of DNA by spectral profile analysis. Ni exposure impaired root meristems as evidenced by the formation of epidermis cell damage, flattened cell nucleus, thickened cortex cell wall, and blurry vascular tissue. Substantial recovery was seen in all parameters with the co-administration of PSEx and Ni. Recovery effects in the parameters were 18–51