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<p>Overproduction of reactive oxygen species (ROS) causes oxidative stress, which is a significant risk factor for the onset and advancement of atherosclerosis. However, in current study, rats with experimentally generated atherosclerosis (EA) are used to examine the effects of prolonged cobalt nitrate exposure on oxidative stress and hematological markers. An atherogenic diet, methylprednisolone, alcohol, and mercazolil were all used in a polyetiological method to imitate atherosclerosis. In the following 60&#xa0;days, rats were given drinking water containing 2&#xa0;mg/kg of cobalt nitrate. The following oxidative stress markers were examined: hematological indices, diene conjugates (DC), catalase (CA), and malondialdehyde (MDA) at baseline, after EA induction, and during cobalt exposure. However, Significant oxidative imbalance was caused on by EA alone, which increased MDA (18%) and DC (20%) while decreasing CA activity (22%). By day 60, cobalt exposure amplified these effects, leading to a decrease in CA (27%) and increasing increases in MDA (64%) and DC (35%). Hematologically, EA first increased granulocytes (1.2 ×), leukocytes (1.8 ×), and lymphocytes (1.3 ×), which were indicative of systemic inflammation. Cobalt, however, overcomes these patterns, gradually causing hemoglobin depletion, erythrocytopenia, and leukopenia. Hemoglobin and mean corpuscular hemoglobin (MCH) dropped by 24% and 25%, respectively, by day 60, suggesting that erythropoiesis and iron metabolism were compromised. The investigation emphasizes that cobalt complicates oxidative stress and blood abnormalities associated with atherosclerosis. Chronic exposure contributes to vascular damage through oxidative and inflammatory mechanisms, even at subtoxic concentrations, exposing people with cardiovascular diseases at risk. In addition to offering treatment options for oxidative stress and hematopoietic support, it emphasizes the necessity of tracking cobalt exposure in at-risk populations. It is advised to conduct additional research and reevaluate the cobalt safety limits.</p>

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Uncovering the oxidative stress and hematological consequences of chronic cobalt exposure on atherosclerosis

  • 期刊论文

  • 发表日期：

    2025年7月15日

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  • Rashad Ibragimov,
  • Rovshan Khalilov,
  • Fidan Nuriyeva,
  • Ilgiz Gareev,
  • Ozal Beylerli,
  • Sergey Roumiantsev,
  • Muhammad Zafar,
  • Deema Kamal Sabir,
  • Salman Majeed,
  • Muhammad Rizwan Khan,
  • Aleena Gul,
  • Jonida Biturku

摘要

Overproduction of reactive oxygen species (ROS) causes oxidative stress, which is a significant risk factor for the onset and advancement of atherosclerosis. However, in current study, rats with experimentally generated atherosclerosis (EA) are used to examine the effects of prolonged cobalt nitrate exposure on oxidative stress and hematological markers. An atherogenic diet, methylprednisolone, alcohol, and mercazolil were all used in a polyetiological method to imitate atherosclerosis. In the following 60 days, rats were given drinking water containing 2 mg/kg of cobalt nitrate. The following oxidative stress markers were examined: hematological indices, diene conjugates (DC), catalase (CA), and malondialdehyde (MDA) at baseline, after EA induction, and during cobalt exposure. However, Significant oxidative imbalance was caused on by EA alone, which increased MDA (18%) and DC (20%) while decreasing CA activity (22%). By day 60, cobalt exposure amplified these effects, leading to a decrease in CA (27%) and increasing increases in MDA (64%) and DC (35%). Hematologically, EA first increased granulocytes (1.2 ×), leukocytes (1.8 ×), and lymphocytes (1.3 ×), which were indicative of systemic inflammation. Cobalt, however, overcomes these patterns, gradually causing hemoglobin depletion, erythrocytopenia, and leukopenia. Hemoglobin and mean corpuscular hemoglobin (MCH) dropped by 24% and 25%, respectively, by day 60, suggesting that erythropoiesis and iron metabolism were compromised. The investigation emphasizes that cobalt complicates oxidative stress and blood abnormalities associated with atherosclerosis. Chronic exposure contributes to vascular damage through oxidative and inflammatory mechanisms, even at subtoxic concentrations, exposing people with cardiovascular diseases at risk. In addition to offering treatment options for oxidative stress and hematopoietic support, it emphasizes the necessity of tracking cobalt exposure in at-risk populations. It is advised to conduct additional research and reevaluate the cobalt safety limits.