article · Toxicology Research
Gibberellic acid is a widely used plant growth regulator in agriculture, but its toxic impacts on mammalian health are not well documented. Exposure in rats leads to substantial liver and kidney damage marked by increased oxidative stress, elevated injury markers, tissue damage, and depleted antioxidant levels. Pre-treatment with chrysin, a natural flavonoid, effectively counteracts these adverse hepatorenal effects. In an animal model, chrysin administration restored organ function markers and key antioxidants, including catalase and glutathione, back to normal levels. At the molecular level, chrysin upregulated protective antioxidant and anti-apoptotic pathways while downregulating inflammatory cytokines and markers of cellular death. It also mitigated histopathological damage within liver and kidney tissues by regulating specific metabolic enzymes and cellular receptors, demonstrating clear protective actions against chemical-induced oxidative injury.
Plant growth regulators are extensively applied in modern agriculture, yet their toxicological risks to vital organs remain insufficiently characterised. Demonstrating how gibberellic acid harms the liver and kidneys, while identifying that the flavonoid chrysin can prevent this damage, provides vital insight into agrochemical safety. It also highlights potential biological targets for protecting individuals frequently exposed to agricultural chemicals.
This research could inform the development of protective nutraceuticals or therapeutic formulations targeting chemical-induced liver and kidney damage. Potential users include pharmaceutical and nutritional supplement developers interested in organ-protective compounds. However, the evidence is derived entirely from an early-stage animal study in rats, meaning clinical safety and efficacy trials in humans would be necessary before any real-world healthcare application could emerge.
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Gibberellic acid (GA3), a widely known plant growth regulator, has been mostly used in agriculture. Little is known regarding its toxicity or the impact of its metabolic mechanism on human health. The current study examined the protective impact of chrysin against GA3-induced liver and kidney dysfunctions at biochemical, molecular, and histopathological levels. Forty male albino rats were allocated into 4 groups. The control group received saline; the chrysin group received 50 mg/kg/BW orally daily for 4 weeks; the GA3 group received 55 mg/kg/BW GA3 via daily oral gavage for 4 weeks, and the protective group (chrysin + GA3) was administered both chrysin and GA3 at the same dosage given in chrysin and GA3 groups. Chrysin was administered 1 h earlier than GA3. The GA3 induced liver and kidney injuries as proven by the elevation of hepatic and renal markers with a significant increase in malondialdehyde levels. Furthermore, a decrease of catalase and glutathione was reported in the GA3-administered rats. Pre-administration of chrysin significantly protected the hepatorenal tissue against the deleterious effects of GA3. Chrysin restored the hepatorenal functions and their antioxidant ability to normal levels. Moreover, chrysin modulated the hepatorenal toxic effects of GA3 at the molecular level via the upregulation of the antiapoptotic genes, interleukin-10 (IL-10), hemoxygenase-1, and nuclear factor erythroid 2-related factor 2 expressions; the downregulation of the kidney injury molecule-1 and caspase-3 mRNA expressions; and a decrease in IL-1β and tumor necrosis factor-α secretions. Additionally, the pre-administration of chrysin effectively attenuated the GA3-induced hepatorenal histopathological changes by regulating the immunoexpression of cytochrome P450 2E1 (CYP2E1) and pregnane X receptor, resulting in normal values at the cellular level. In conclusion, chrysin attenuated GA3-induced oxidative hepatorenal injury by inhibiting free-radical production and cytokine expression as well as by modulating the antioxidant, apoptotic, and antiapoptotic activities. Chrysin is a potent hepatorenal protective agent to antagonize oxidative stress induced by GA3.
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DOI: 10.1093/toxres/tfac003
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