Glyphosate-based herbicides, the most extensively used herbicides in the world, are available in an enormous number of commercial formulations with varying additives and adjuvants. Here, we study the effects of one such formulation, Credit41, in two genetically diverse yeast strains. A quantitative trait loci (QTL) analysis between a sensitive laboratory strain and a resistant strain linked mitochondrial function to Credit41 resistance. Two genes encoding mitochondrial proteins identified through the QTL analysis were HFA1, a gene that encodes a mitochondrial acetyl CoA carboxylase, and AAC3, which encodes a mitochondrial inner membrane ATP/ADP translocator. Further analysis of previously studied whole-genome sequencing data showed that, although each strain uses varying routes to attain glyphosate resistance, most strains have duplications of mitochondrial genes. One of the most well-studied functions of the mitochondria is the assembly of Fe–S clusters. In the current study, the expression of iron transporters in the transcriptome increased in cells resistant to Credit41. The levels of iron within the cell also increased in cells exposed to Credit41 but not pure glyphosate. Hence, the additives in glyphosate-based herbicides have a significant contribution to the negative effects of these commercial formulations on biological systems.

The goal of this work was to understand the extent of mercury toxic effects in liver metabolism under an episode of acute contamination. Hence, the effects of in vitro mercuric chloride in liver mitochondria were assessed in two commercial marine fish: Senegalese sole (Solea senegalensis) and gilthead seabream (Sparus aurata). Liver mitochondria were exposed to 0.2mgL−1 of mercury, the average concentration found in fish inhabiting contaminated areas. Mercuric chloride depressed mitochondrial respiration state 3 and the maximal oxygen consumption in the presence of FCCP indicating inhibitory effects on the oxidative phosphorylation and on the electron transport chain, respectively. The inhibition of F1Fo-ATPase and succinate-dehydrogenase activities also corroborated the ability of mercury to inhibit ADP phosphorylation and the electron transport chain. This study brings new understanding on the mercury levels able to impair fish mitochondrial function, reinforcing the need for further assessing bioenergetics as a proxy for fish health status.

The effects of exogenous ascorbic acid (AsA) on the growth parameters, nitrogen metabolism, energy status, and photosynthetic gas exchange in alfalfa under high-nitrate stress were studied. The seedlings treated with the control, 200 mmol L⁻¹ nitrates (HN) or 200 mmol L⁻¹ nitrate + 0.1 mmol L⁻¹ AsA (HN + AsA), were sampled on days 0 and 10 after treatments. AsA was sprayed on the leaves, while HN was conducted by watering. Both of them were performed once every other day for three times in total. The results revealed that in the HN treatment, the growth parameters were the lowest; total phosphorus (TP), nitrogen-related enzyme activities, soluble protein (SP), adenosine triphosphate (ATP), and energy charge (EC) were reduced; and photosynthetic rate (Photo), conductance to H₂O (Cond), transpiration rate (Trmmol), instantaneous water use efficiency (WUE), and apparent CO₂ use efficiency (CUE) were also inhibited; and total nitrogen (TN), nitrate-nitrogen (NO₃¯-N), ammonium-nitrogen (NH₄⁺-N), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and intercellular CO₂ concentration (Ci) were increased compared with the control. However, these parameters changed conversely in the HN + AsA treatment. In addition, there was a good curve regression equation relationship between TN and NO₃¯-N, TN and NH₄⁺-N, NO₃¯-N and NH₄⁺-N, respectively. It indicates that AsA improves the growth parameters, nitrogen-related enzyme activities, energy metabolism, and photosynthesis, whereas it inhibits the toxicity of excess NO₃¯-N and NH₄⁺-N accumulations, thereby promoting the growth of alfalfa under high-nitrate stress. These metabolisms are closely related to each other during the regulatory process in alfalfa. Hence, AsA has potential to be applied to improve the growth of alfalfa under high-nitrate stress.

The purpose of this review is to describe how plants take up lead and its distribution to plant parts, morphological, physiological, and biological effects of lead on plants, sequestration strategies, and tolerance mechanisms including detoxification. How lead despite its lack of essential function in plants, causes phytotoxicity by changing cell membrane permeability, by reacting with active groups of different enzymes involved in plant metabolism by reacting with the phosphate groups of adenosine diphosphate (ADP) or adenosine-5′-triphosphate (ATP). Moreover, we also address role of hyperaccumulating plants in lead absorption. How synthetic chelators such as ethylenediaminetetraacetic acid (EDTA) enhances the availability of heavy metal lead in soils and increase phytoextraction efficiency in aboveground harvestable plant parts through enhancing the metal solubility and translocation from roots to shoots, metal tolerance, and future prospectives to decrease lead pollution.