Measures of manganese (Mn) status in cattle vary among studies, and no single criterion accurately predicts or diagnoses Mn deficiency and pathologic outcomes. Mn deficiency causes congenital joint laxity and dwarfism (CJLD) when total dietary intake is <20 ppm Mn dry matter (DM) for most of the pregnancy. However, the recommended dietary intake of 40 ppm DM can also result in clinical Mn deficiency. Some studies have found that CJLD occurs in calves from cows fed red clover or silage but not in calves from cows fed hay. The concentration of Mn in the liver is the best indicator of Mn status in neonates and adults but cannot be interpreted in fetuses. Serum, plasma, and whole blood concentrations of Mn are unreliable indicators of bovine Mn status. The primary objective of our report is to present evidence linking CJLD to a primary or secondary Mn deficiency. To predict and diagnose Mn deficiency in cattle, we propose using a combination of clinical signs, dietary Mn, liver Mn at birth and beyond, positive response to Mn supplementation or the replacement of silage with other forages, and ruling out other causes of malformations. By following these recommendations, we expect that CJLD and gestational death will decrease as hepatic Mn concentrations increase at birth. Many publications we reviewed are not statistically sound, and future research should include a statistician from the initial discussions of the study through the final publication.

This brief article highlights the results of Fu et al. (Proc Natl Acad Sci USA 119:e2204574119, 2022), who recently found that manganese (Mn) deficiency triggers long-lasting multicellular Ca2+ oscillations in the elongation zone (EZ) of Arabidopsis roots and revealed a Ca2+-CPK21/23-NRAMP1 axis as an important mechanism for plant tolerance and adaptation to low Mn.

In this work, we investigated cases of birth of calves with congenital defects in a farm in Southern Brazil. Only calves born from heifers were affected, and the disease occurred in both crossbred and purebred calves. Three necropsies were performed, tissues were collected for histopathology, and samples of liver of calves, blood serum, and food provided for cows and heifers were collected to quantify the levels of the minerals: manganese, copper, and zinc. The calves were born weak, with disproportionate dwarfism, limb deformities, and enlarged joints. Heads were shortened and domed. Long bones had a shortened diaphysis and a normal-sized epiphysis, when compared to the control. In one of the cases, there were white-yellowish lines on the metaphyseal surface of the epiphyseal plate. Histopathology of growth plates revealed premature closure, disarrangement of chondrocyte columns, and collapse of primary spongiosa. These findings supported a diagnosis of chondrodysplasia. Liver manganese levels were under the reference values in the three calves. Food analysis revealed insufficient levels of manganese in the diet of heifers, especially in sorghum silage, which was provided as the main source of food for the category in some periods. Approximately 6 months after the diet was changed, the problem ceased and only normal calves continued to be born. Our findings allowed to conclude the diagnosis of chondrodysplasia of nutritional origin and reinforce the thesis that manganese is the mineral deficient in these cases.

Manganese (Mn) is an essential trace element for bone growth, and its deficiency has been shown to increase the incidence of leg abnormalities in fast-growing broilers, such as tibial dyschondroplasia (TD). Proliferation and differentiation of growth plate chondrocyte are critical for tibia development, but their roles in Mn deficiency-induced TD remains to be elucidated. Thirty 1-day-old Arbor Acres chicks were randomly divided into two groups and fed with control diet (60 mg Mn/kg diet) and Mn-deficiency diet (22 mg Mn/kg diet) for 42 days, respectively. Mn deficiency-induced TD model was successfully established and samples from proximal tibia metaphysis and growth plate were collected for assays. Pathological observation showed that Mn deficiency induced morphological abnormality and irregular arrangement of chondrocytes in proliferative and hypertrophic zone of tibial growth plate. Also, Mn deficiency decreased mRNA and protein expression levels of type II collagen and type X collagen in tibial growth plate, indicating the impairment of proliferating and hypertrophic chondrocytes. Moreover, down-regulated gene expression levels of Sox9, Tgf-β, Ihh, Runx2, Mef2c and Bmp-2 were shown in tibial growth plate of Mn-deficiency group, demonstrating that Mn deficiency inhibited the transcription levels of key regulators to disrupt chondrocyte proliferation and differentiation. Collectively, these findings confirmed that Mn deficiency affected the proliferation and differentiation of chondrocytes in tibial growth plate via inhibiting related regulatory factors, leading to TD in broilers.

Manganese (Mn) is an important micronutrient for plant growth and development and sustains metabolic roles within different plant cell compartments. The metal is an essential cofactor for the oxygen-evolving complex (OEC) of the photosynthetic machinery, catalyzing the water-splitting reaction in photosystem II (PSII). Despite the importance of Mn for photosynthesis and other processes, the physiological relevance of Mn uptake and compartmentation in plants has been underrated. The subcellular Mn homeostasis to maintain compartmented Mn-dependent metabolic processes like glycosylation, ROS scavenging, and photosynthesis is mediated by a multitude of transport proteins from diverse gene families. However, Mn homeostasis may be disturbed under suboptimal or excessive Mn availability. Mn deficiency is a serious, widespread plant nutritional disorder in dry, well-aerated and calcareous soils, as well as in soils containing high amounts of organic matter, where bio-availability of Mn can decrease far below the level that is required for normal plant growth. By contrast, Mn toxicity occurs on poorly drained and acidic soils in which high amounts of Mn are rendered available. Consequently, plants have evolved mechanisms to tightly regulate Mn uptake, trafficking, and storage. This review provides a comprehensive overview, with a focus on recent advances, on the multiple functions of transporters involved in Mn homeostasis, as well as their regulatory mechanisms in the plant\'s response to different conditions of Mn availability.

A dune forest in SW France composed of maritime pines was irrigated with treated wastewater for a decade in an experiment (including irrigated plots versus control plots) to evaluate the environmental impact of applying wastewater on the water table, soil properties, and plants. The amount of treated wastewater (1921 mm yr-1) applied was twice the annual precipitation. Nutrient inputs were also very high, particularly nitrogen (N: 539 kg-N ha-1 yr-1), phosphorus (P: 102 kg-P ha-1 yr-1), and calcium (Ca: 577 kg-Ca ha-1 yr-1). Irrigation caused a rise in the water table, and increased its sodium (Na), NO3-, potassium (K), and calcium concentrations. Soil properties were affected by irrigation at least down to a depth of 1.2 m. After eight years of irrigation, soil pH had increased by 1.4 units, and soil available P content (POlsen) increased nearly 8-fold. In the short-term (i.e. 1-3 years), irrigation with treated wastewater improved growth, standing biomass, and the nutritional status of the vegetation. But tree dieback started in the fourth year of irrigation and worsened until the end of the monitoring period when almost all the irrigated trees were dead or moribund. The understory composition was drastically modified by irrigation, with an increase in α-biodiversity and in the biomass of herbaceous species, and a reduction in woody species abundance. The factor that best explained tree dieback was manganese nutrition (Mn): (i) the Mn content of the tree foliage was negatively affected by irrigation and below the deficiency values reported for pine species, and (ii) soil available Mn (CaCl2 extraction) decreased by half in the topsoil layer. Manganese deficiency was probably the consequence of the increase in soil pH, which in turn reduced soil Mn availability. Tree dieback was not related to either to a macronutrient deficiency or to toxicity caused by a trace element.

Manganese (Mn) is an essential micronutrient required for the activity of metalloenzymes. It is an essential component of parenteral nutrition (PN), but requirements are low. Mn status is difficult to assess, with the commonest method being measurement of its concentration in whole blood. This method has limitations, including artifactually high concentrations resulting from contamination of specimen tubes. Mn toxicity is a well-recognized complication of PN, the risk of which increases if there is cholestasis or if the patient has received high doses. It usually presents with parkinsonian-like symptoms but may be detected presymptomatically as hypermanganesemia or as increased signal intensity of the basal ganglia upon T1-weighted magnetic resonance imaging. Caution is necessary when providing Mn for patients on long-term PN (>1 month). It is advisable to withhold supplementation if hypermanganesemia or cholestasis develops. Deficiency of Mn is rare in patients treated with PN. PN regimens are contaminated with Mn in amounts likely to meet requirements. Consequently, it is debated whether PN should be routinely supplemented with Mn. The currently recommended dose of Mn in adults treated with PN is 55 μg/d, but the doses provided by most currently available multi-trace element products exceed this. In response to calls for new products to be developed, 2 new multi-trace element products are currently available in Europe that provide Mn doses of 55 μg/d. Once these products are in general use, it is likely that the incidence of Mn toxicity will decrease.

Manganese (Mn) constitutes an essential co-factor in the oxygen-evolving complex of photosystem II (PSII). Consequently, Mn deficiency reduces photosynthetic efficiency and leads to changes in PSII composition. In order to study these changes, multiplexed protein assays are advantageous. Here, we developed a multiplexed antibody-based assay and analysed selected PSII subunits in barley (Hordeum vulgare L.). A selection of antibodies were labelled with specific lanthanides and immunoreacted with thylakoids exposed to Mn deficiency after western blotting. Subsequently, western blot membranes were analysed by laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS), which allowed selective and relative quantitative analysis via the different lanthanides. The method was evaluated against established liquid chromatography electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) methods, based on data-dependent acquisition (DDA) and selected reaction monitoring (SRM). Manganese deficiency resulted in a general decrease in PSII protein abundances, an effect that was shown to be reversible upon Mn re-supplementation. Specifically, the extrinsic proteins PsbP and PsbQ showed Mn-dependent changes in abundances. Similar trends in the response to Mn deficiency at the protein level were observed when comparing DDA, SRM and LA-ICP-MS results. A biologically important exception to this trend was the loss of PsbO in the SRM analysis, which highlights the necessity of validating protein changes by more than one technique. The developed method enables a higher number of proteins to be multiplexed in comparison to existing immunoassays. Furthermore, multiplexed protein analysis by LA-ICP-MS provides an analytical platform with high throughput appropriate for screening large collections of plants.

The occurrence of manganese (Mn) deficiency in cereal crops has increased in recent years. This coincides with increasing phosphorus (P) status of many soils due to application of high levels of animal manure and P-fertilizers. In order to test the hypothesis that elevated P my lead to Mn deficiency we have here conducted a series of hydroponics and soil experiments examining how the P supply affects the Mn nutrition of barley. Evidence for a direct negative interaction between P and Mn during root uptake was obtained by on-line inductively coupled plasma mass spectrometry (ICP-MS). Addition of a pulse of KH(2)PO(4) rapidly and significantly reduced root Mn uptake, while a similar concentration of KCl had no effect. Addition of a P pulse to the same nutrient solution without plants did not affect the concentration of Mn, revealing that no precipitation of Mn-P species was occurring. Barley plants growing at a high P supply in hydroponics with continuous replenishment of Mn(2+) had up to 50% lower Mn concentration in the youngest leaves than P limited plants. This P-induced depression of foliar Mn accelerated the development of Mn deficiency as evidenced by a marked change in the fluorescence induction kinetics of chlorophyll a. Also plants growing in soil exhibited lower leaf Mn concentrations in response to elevated P. In contrast, leaf concentrations of Fe, Cu, and N increased with the P supply, supporting that the negative effect of P on Mn acquisition was specific rather than due to a general dilution effect. It is concluded that elevated P supply directly interferes with Mn uptake in barley roots and that this negative interaction can induce Mn deficiency in the shoot. This finding has major implications in commercial plant production where many soils have high P levels.