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<p>In this study, the toxicity induced by metronidazole, one of the most preferred pharmaceutical active ingredients worldwide, in <i>Allium cepa</i> L, a non-target organism, was investigated. Many genetic (mitotic index = MI, micronucleus = MN and chromosomal abnormalities = CAs) and biochemical (malondialdehyde = MDA, proline, superoxide dismutase = SOD, catalase = CAT, chlorophyll a and b) parameters have been used as indicators of toxicity. Furthermore, the degree of DNA damage caused by metronidazole was investigated by the Comet assay method. On the other hand, metronidazole toxicity was also supported using the in silico method in a computer environment. Four groups of <i>A. cepa</i> bulbs were created, including three treatments and a control. Metronidazole doses of 125, 250, and 500&#xa0;mg/L were used to germinate the onions in the treatment groups, while tap water was used to germinate the onions in the control group. Samples taken from roots and leaves were used in measurements and physiological examinations. Consequently, the maximum MI value and chlorophyll amounts were measured in the control group. In addition, the lowest MN and CAs numbers, MDA and proline levels, and SOD and CAT activities were also measured in this group. Metronidazole exposure caused notable (<i>p</i> &lt; 0.05) declines in MI value and chlorophyll amounts, and notable increases (<i>p</i> &lt; 0.05) in MN and CAs numbers, MDA and proline levels, and SOD and CAT activities, depending on the dose. Metronidazole exposure promoted CAs such as sticky chromosome, bridge, vagrant chromosome, nuclear bud, and binuclear cell in root meristem cells. Comet assay findings revealed significant decreases (<i>p</i> &lt; 0.05) in the percentage of head DNA and significant increases (<i>p</i> &lt; 0.05) in the percentage of tail DNA depending on the metronidazole dose, and this indicated DNA damage. The in silico study’s findings supported the genetic and biochemical toxicity results by showing the direct interaction of metronidazole with DNA, tubulin proteins, topoisomerase enzymes and enzymes responsible for chlorophyll synthesis. Consequently, it has been demonstrated that metronidazole may cause multifaceted toxicity in non-target organisms if it goes beyond its medical use and spreads into the environment. In addition, once more, it has been established that <i>A. cepa</i> is a trustworthy indicator organism for figuring out this toxicity.</p>

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Investigation of in-vivo and in-silico toxicity induced by environmental drug contamination in a non-target organism

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月1日

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  • Numan Annakkaya,
  • Kültiğin Çavuşoğlu,
  • Emine Yalçin,
  • Burak Özkan

摘要

In this study, the toxicity induced by metronidazole, one of the most preferred pharmaceutical active ingredients worldwide, in Allium cepa L, a non-target organism, was investigated. Many genetic (mitotic index = MI, micronucleus = MN and chromosomal abnormalities = CAs) and biochemical (malondialdehyde = MDA, proline, superoxide dismutase = SOD, catalase = CAT, chlorophyll a and b) parameters have been used as indicators of toxicity. Furthermore, the degree of DNA damage caused by metronidazole was investigated by the Comet assay method. On the other hand, metronidazole toxicity was also supported using the in silico method in a computer environment. Four groups of A. cepa bulbs were created, including three treatments and a control. Metronidazole doses of 125, 250, and 500 mg/L were used to germinate the onions in the treatment groups, while tap water was used to germinate the onions in the control group. Samples taken from roots and leaves were used in measurements and physiological examinations. Consequently, the maximum MI value and chlorophyll amounts were measured in the control group. In addition, the lowest MN and CAs numbers, MDA and proline levels, and SOD and CAT activities were also measured in this group. Metronidazole exposure caused notable (p < 0.05) declines in MI value and chlorophyll amounts, and notable increases (p < 0.05) in MN and CAs numbers, MDA and proline levels, and SOD and CAT activities, depending on the dose. Metronidazole exposure promoted CAs such as sticky chromosome, bridge, vagrant chromosome, nuclear bud, and binuclear cell in root meristem cells. Comet assay findings revealed significant decreases (p < 0.05) in the percentage of head DNA and significant increases (p < 0.05) in the percentage of tail DNA depending on the metronidazole dose, and this indicated DNA damage. The in silico study’s findings supported the genetic and biochemical toxicity results by showing the direct interaction of metronidazole with DNA, tubulin proteins, topoisomerase enzymes and enzymes responsible for chlorophyll synthesis. Consequently, it has been demonstrated that metronidazole may cause multifaceted toxicity in non-target organisms if it goes beyond its medical use and spreads into the environment. In addition, once more, it has been established that A. cepa is a trustworthy indicator organism for figuring out this toxicity.