<p>Chlorpyrifos (CPF), a widely used organophosphorus pesticide, induces adverse effects such as organ toxicity, endocrine disruption, oxidative stress, and histopathological damage in non-target organisms. Emerging evidence suggests that lactic acid bacteria (LABs) can alleviate CPF-induced tissue damage. This study investigated the protective effects of probiotic lactobacilli against subacute CPF toxicity in the heart and lungs of rats. Eight groups of male Sprague‒Dawley rats were exposed to CPF and probiotics for 6 weeks. CPF toxicity triggered lipid peroxidation, evidenced by a 40% and 60% rise in malondialdehyde (MDA) levels in heart and lung tissues, respectively. Additionally, CPF significantly elevated superoxide dismutase (SOD) and IL-1β, indicating oxidative and pro-inflammatory responses. Probiotic treatment effectively suppressed CPF-induced increases in MDA, SOD, and IL-1β. Histopathological analysis demonstrated that <i>Lactobacillus acidophilus</i> (heart) and <i>Lactobacillus casei</i> (lungs), particularly the probiotic bacterial mixture in each respective tissue, attenuated CPF-induced tissue damage. In conclusion, probiotic supplementation mitigates CPF-mediated cardiotoxicity and pulmonary toxicity by modulating antioxidant and inflammatory pathways.</p>

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Probiotic Lactobacillus Strains Mitigate Chlorpyrifos-Induced Lung and Heart Toxicity in Rats via Anti-inflammatory and Antioxidant Mechanisms

  • Hiva Alipanah,
  • Ziba Sohrabi,
  • Mehran Sayadi,
  • Amene Nematollahi,
  • Roghayeh Nejati

摘要

Chlorpyrifos (CPF), a widely used organophosphorus pesticide, induces adverse effects such as organ toxicity, endocrine disruption, oxidative stress, and histopathological damage in non-target organisms. Emerging evidence suggests that lactic acid bacteria (LABs) can alleviate CPF-induced tissue damage. This study investigated the protective effects of probiotic lactobacilli against subacute CPF toxicity in the heart and lungs of rats. Eight groups of male Sprague‒Dawley rats were exposed to CPF and probiotics for 6 weeks. CPF toxicity triggered lipid peroxidation, evidenced by a 40% and 60% rise in malondialdehyde (MDA) levels in heart and lung tissues, respectively. Additionally, CPF significantly elevated superoxide dismutase (SOD) and IL-1β, indicating oxidative and pro-inflammatory responses. Probiotic treatment effectively suppressed CPF-induced increases in MDA, SOD, and IL-1β. Histopathological analysis demonstrated that Lactobacillus acidophilus (heart) and Lactobacillus casei (lungs), particularly the probiotic bacterial mixture in each respective tissue, attenuated CPF-induced tissue damage. In conclusion, probiotic supplementation mitigates CPF-mediated cardiotoxicity and pulmonary toxicity by modulating antioxidant and inflammatory pathways.