This study aimed to test the efficiency of ethylene (Eth; 200 µL L⁻¹ ethephon) in presence or absence of nitrogen (N; 80 mg N kg⁻¹ soil) in protecting photosynthetic apparatus from copper (Cu; 100 mg Cu kg⁻¹ soil) stress in mustard (Brassica juncea L.) and to elucidate the physio-biochemical modulation for Eth plus N-induced Cu tolerance. Elevated Cu-accrued reductions in photosynthesis and growth were accompanied by significantly higher Cu accumulation in leaves and oxidative stress with reduced assimilation of N and sulfur (S). Ethylene in coordination with N considerably reduced Cu accumulation, lowered lipid peroxidation, lignin accumulation, and contents of reactive oxygen species (hydrogen peroxide, H₂O₂, and superoxide anion, O₂•⁻), and mitigated the negative effect of Cu on N and S assimilation, accumulation of non-protein thiols and phytochelatins, enzymatic, and non-enzymatic antioxidants (activity of ascorbate peroxidase, APX, and glutathione reductase, GR; content of reduced glutathione, GSH, and ascorbate, AsA), cell viability, photosynthesis, and growth. Overall, the effect of ethylene-nitrogen synergism was evident on prominently mitigating Cu stress and protecting photosynthesis. The approach of supplementing ethylene with N may be used as a potential tool to restrain Cu stress, and protect photosynthesis and growth of mustard plants.

Ethephon is an organophosphorus plant growth regulator used to accelerate the ripening process and decrease the duration of cultivation. Here, the potential protective role of aged garlic extract (AGE) was investigated against ethephon-mediated nephrotoxicity. Four experimental groups were established (n = 15), including control, AGE (250 mg/kg), ethephon (200 mg/kg), and AGE + ethephon. In the current work, kidney function parameters (urea, creatinine, and KIM-1) along with oxidative stress biomarkers, nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1, glutathione, and its related enzymes, superoxide dismutase, catalase, malondialdehyde, and nitric oxide, were determined. The expression of inflammatory mediators namely tumor necrosis factor alpha, interleukin 1 beta, nuclear factor kappa B, and apoptotic markers (caspase 3, Bax, and Bcl2) were determined in the renal tissue. Additionally, the histopathological alterations in response to treatments were examined. Ethephon exposure increased the levels of kidney function markers along with relative kidney weight coupled with histological changes in the kidney tissue. Additionally, ethephon increased the levels of the tested pro-oxidant markers and decreased the antioxidant indices, resulting in oxidative damage to renal tissues. An elevation in the pro-inflammatory mediators was also recorded following ethephon intoxication. Furthermore, renal cell loss was observed through histological examinations and biochemical measurements upon ethephon administration. On the other hand, AGE significantly ameliorated the molecular, biochemical, and structural changes elicited by ethephon. These findings suggest that AGE may be used to decrease or prevent the side effects of ethephon exposure in kidneys, through the activation of Nrf2 and inhibition of inflammation and apoptotic response.

The current study was designed to demonstrate the hepatoprotective effect of aged garlic extract (AGE) against ethephon-induced liver toxicity in rats. Sixty male Wistar albino rats were divided into four groups as follows: the control group; AGE group was administered with 250 mg/kg; the ethephon group was orally given 200 mg/kg; and AGE + ethephon group was treated with ethephon for 4 weeks and then given AGE for another 4 weeks using the same dosage. The ethephon administration impaired the balance between oxidants and antioxidants as evidenced by the increased level of malondialdehyde (MDA) and the decreased concentration of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Biochemical findings showed a significant decrease in the red blood corpuscles (RBCs) count, hemoglobin (Hb) content, and hematocrit (HCT) level, with a significant increase in the white blood cells count. In addition, ethephon produced a significant decrease in levels of aspartate transaminase (AST) and alanine transaminase (ALT) with a decrease in albumin level. Furthermore, histological investigation showed dilation of the hepatic central vein and dilation of blood sinusoids which were congested with inflammatory cellular infiltrate. Moreover, examination of the liver using transmission electron microscopy showed a disturbance in the nuclear membranes and degenerating mitochondria with a rise in the cytoplasmic vacuoles by cellular edema. Interestingly, AGE administration was found to attenuate the histological deformations and biochemical alteration produced by ethephon. These findings suggest that AGE supplementation could be used to reverse the hepatic injury following ethephon exposure through its antioxidant capacity.