Association between health literacy and dysphagia in the community-dwelling older population: a cross-sectional study.

BACKGROUND: Dysphagia, or swallowing disorders, has become a growing concern due to the aging population, and health literacy plays a crucial role in active aging. However, the relationship between them remains unclear. AIMS: To investigate the association between health literacy and dysphagia among community-dwelling older adults in China. METHODS: A survey was conducted on 4462 older adults aged 65 and above in a community in Yiwu City, China, from May 2021 to January 2022. Swallowing problems were assessed using a 30 ml water swallowing test (WST) and the Eating Assessment Tool-10 questionnaire (EAT-10). The participants' health literacy was evaluated using the Chinese Health Literacy Scale (CHLS). Logistic regression and t tests were employed to measure the association between them. RESULTS: The prevalence of dysphagia was 5.70% and 7.85% as determined by EAT-10 and 30 ml-WST, respectively. The health literacy level of community-dwelling older adults was 24.4 ± 4.93 (9-45). Participants with dysphagia exhibited lower levels of health literacy (p < 0.05). The logistic regression model demonstrated an inverse association between health literacy and dysphagia (OR = 0.94, 95%CI = 0.91-0.96 for EAT-10, and OR = 0.93, 95%CI = 0.92-0.95 for WST). Moreover, this association remained significant even after adjusting for covariates. DISCUSSION: Older adults with dysphagia have lower levels of health literacy, particularly in terms of their ability to seek medical advice, acquire and evaluate medical information, and access social support resources. CONCLUSIONS: Health literacy is associated with dysphagia among community-dwelling older adults. Effective interventions should be implemented to provide support in terms of both medical services and social support for this population.

Titanium dioxide nanoparticles relieve biochemical dysfunctions of fifth-instar larvae of silkworms following exposure to phoxim insecticide.

Phoxim insecticide is widely used in agriculture, which is toxic to insect pests and nontarget organisms. The phoxim poisoning is hard to prevent for silkworms. TiO(2) NPs have been widely applied in whitening, brightening foods, toothpaste or sunscreens, and orally-administered drugs. However, whether TiO(2) NPs can increase resistance of silkworm to phoxim poisoning has not been reported. The results demonstrated that added TiO(2) NPs significantly decreased reduction of protein, glucose and pyruvate contents, lactate dehydrogenase, succinate dehydrogenase and malate dehydrogenase activities, and attenuated increases of free amino acids, urea, uric acid and lactate levels, activities of protease, alanine aminotransferase and aspartate aminotransferase in the hemolymph of silkworms caused by phoxim exposure. From the present study, it is clearly evident that added TiO(2) NPs may relieve toxic impacts of phoxim insecticide on silkworm metabolism, which in turn may result in an increase in silk yield.

Cerium chloride improves protein and carbohydrate metabolism of fifth-instar larvae of Bombyx mori under phoxim toxicity.

The organophosphorus pesticide poisoning of the silkworm Bombyx mori is one of the major events causing serious damage to sericulture. Added low-dose rare earths are demonstrated to increase resistance in animals. However, very little is known about whether or not added CeCl3 can increase resistance of silkworm to phoxim poisoning. The present findings suggested that added CeCl3 to mulberry leaves markedly increased contents of protein, glucose and pyruvate, and carbohydrate metabolism-related enzyme activities, including lactate dehydrogenase, succinate dehydrogenase and malate dehydrogenase, and attenuated free amino acids, urea, uric acid and lactate levels and inhibited the protein metabolism-related enzymes activities, such as protease, alanine aminotransferase and aspartate aminotransferase in the haemolymph of B. mori, under phoxim toxicity. These findings suggest that added CeCl3 may improve protein and carbohydrate metabolisms, thus leading to increases of growth and survival rate of B. mori under phoxim stress.

Magnesium deficiency results in damage of nitrogen and carbon cross-talk of maize and improvement by cerium addition.

Magnesium (Mg) deficiency has been reported to affect plant photosynthesis and growth, and cerium (Ce) was considered to be able to improve plant growth. However, the mechanisms of Mg deficiency and Ce on plant growth remain poorly understood. The main aim of this work is to identify whether or not Mg deprivation affects the interdependent nitrogen and carbon assimilations in the maize leaves and whether or not Ce modulates the assimilations in the maize leaves under Mg deficiency. Maize plants were cultivated in Hoagland's solution. They were subjected to Mg deficiency and to cerium chloride administration in the Mg-present Hoagland's media and Mg-deficient Hoagland's media.After 2 weeks,we measured chlorophyll (Chl) a fluorescence and the activities of nitrate reductase (NR), sucrose-phosphate synthase(SPS), and phosphoenolpyruvate carboxylase (PEPCase)in metabolic checkpoints coordinating primary nitrogen and carbon assimilations in the maize leaves. The results showed that Mg deficiency significantly inhibited plant growth and decreased the activities of NR, SPS, and PEPCase and the synthesis of Chl and protein. Mg deprivation in maize also significantly decreased the oxygen evolution, electron transport,and efficiency of photochemical energy conversion by photosystem II (PSII). However, Ce addition may promote nitrogen and carbon assimilations, increase PSII activities,and improve maize growth under Mg deficiency. Moreover,our findings would help promote usage of Mg or Ce fertilizers in maize production.

Signal pathway of hippocampal apoptosis and cognitive impairment of mice caused by cerium chloride.

Experimental studies have demonstrated that lanthanides could impair cognitive functions of children and animals, but very little is known about the hippocampal apoptosis and its molecular mechanism. The study investigated the signal pathway of hippocampal apoptosis induced by intragastric administration of CeCl(3) for 60 consecutive days. It showed that cerium had been significantly accumulated in the mouse hippocampus, and CeCl(3) caused hippocampal apoptosis and impairment of spatial recognition memory of mice. CeCl(3) effectively activated caspase-3 and -9, inhibited Bcl-2, and increased the levels of Bax and cytochrome c, promoted accumulation of reactive oxygen species in the mouse hippocampus. It implied that CeCl(3)-induced apoptosis in the mouse hippocampus could be triggered via mitochondrion-mediated pathway. Our findings suggest the need for great caution to handle the lanthanides for workers and consumers.

Liver injury and its molecular mechanisms in mice caused by exposure to cerium chloride.

Cerium has been demonstrated to damage liver of mice, but very little is known about the molecular mechanisms underlying the mouse liver apoptosis. In order to understand the liver injury induced by intragastric administration of cerium chloride (CeCl3) for 60 consecutive days, the hepatocyte ultrasrtucture, various oxidative stress parameters, and the stress-related gene expression levels were investigated for the mouse liver. The results demonstrated that CeCl3 had an obvious accumulation in the mouse liver, leading to a classical laddering cleavage of DNA and hepatocyte apoptosis. CeCl3 significantly promoted the accumulation of reactive oxygen species and inhibited the stress-related gene expression of superoxide dismutase, catalase, glutathione peroxidase, metallothionein, heat-shock protein 70, glutathione-S-transferase, P53, and transferring, and it effectively activated the cytochrome p450 1A. It implied that CeCl3 resulted in apoptosis and alteration of expression levels of the genes related with metal detoxification/metabolism regulation and radical scavenging action in mice.

Effects of manganese deficiency and added cerium on photochemical efficiency of maize chloroplasts.

The mechanism of the fact that manganese deprivation and cerium addition affect the photochemical efficiency of plants is unclear. In this study, we investigated the improvement by cerium of the damage of the photochemical function of maize chloroplasts under manganese-deprived stress. Chlorophyll fluorescence induction measurements showed that the ratio of variable to maximum fluorescence (Fv/Fm) underwent great decreases under manganese deficiency, which was attributed to the reduction of intrinsic quantum efficiency of the photosystem II units. The electron flow between the two photosystems, activities of Mg(2+)-ATPase and Ca(2+)-ATPase, and rate of photophosphorylation on the thylakoid membrane of maize chloroplasts were reduced significantly by exposure to manganese deprivation. Furthermore, the inhibition of cyclic photophosphorylation was more severe than non-cyclic photophosphorylation under manganese deficiency. However, added cerium could relieve the inhibition of the photochemical reaction caused by manganese deprivation in maize chloroplasts. It implied that manganese deprivation could disturb photochemical reaction of chloroplasts strongly, which could be improved by cerium addition.

Effects of added CeCl3 on resistance of fifth-instar larvae of silkworm to Bombyx mori nucleopolyhedrovirus infection.

One of the most important agents causing lethal disease in the silkworm is the Bombyx mori nucleopolyhedrovirus (BmNPV), while low-dose rare earths are demonstrated to increase immune capacity in animals. However, very little is known about the effects of added CeCl(3) on decreasing BmNPV infection of silkworm. The present study investigated the effects of added CeCl(3) to an artificial diet on resistance of fifth-instar larvae of silkworm to BmNPV infection. Our findings indicated that added CeCl(3) significantly decreased inhibition of growth and mortality of fifth-instar larvae caused by BmNPV infection. Furthermore, the added CeCl(3) obviously decreased lipid peroxidation level and accumulation of reactive oxygen species such as O(2)(-), H(2)O(2), (·)OH, and NO and increased activities of the antioxidant enzymes including superoxide dismutase, catalase, ascorbate peroxidase, glutathione peroxidase, ascorbate, and glutathione contents in the BmNPV-infected fifth-instar larvae. In addition, the added CeCl(3) could significantly promote acetylcholine esterase activity and attenuate the activity of inducible nitric oxide synthase in the BmNPV-infected fifth-instar larvae. These findings suggested that added CeCl(3) may relieve oxidative damage and neurotoxicity of silkworm caused by BmNPV infection via increasing antioxidant capacity and acetylcholine esterase activity.

Effects of manganese deficiency and added cerium on nitrogen metabolism of maize.

Manganese is one of the essential microelements for plant growth, and cerium is a beneficial element for plant growth. However, whether manganese deficiency affects nitrogen metabolism of plants and cerium improves the nitrogen metabolism of plants by exposure to manganese-deficient media are still unclear. The main aim of the study was to determine the effects of manganese deficiency in nitrogen metabolism and the roles of cerium in the improvement of manganese-deficient effects in maize seedlings. Maize seedlings were cultivated in manganese present Meider's nutrient solution. They were subjected to manganese deficiency and to cerium chloride administered in the manganese-present and manganese-deficient media. Maize seedlings grown in the various media were measured for key enzyme activities involved in nitrogen metabolism, such as nitrate reductase, glutamate dehydrogenase, glutamine synthetase, and glutamic-oxaloace transaminase. We found that manganese deficiency restricted uptake and transport of NO(3)(-), inhibited activities of nitrogen-metabolism-related enzymes, such as nitrate reductase, glutamine synthetase, and glutamic-oxaloace transaminase, thus decreasing the synthesis of chlorophyll and soluble protein, and inhibited the growth of maize seedlings. Manganese deficiency promoted the activity of glutamate dehydrogenase and reduced the toxicity of excess ammonia to the plant, while added cerium relieved the damage to nitrogen metabolism caused by manganese deficiency in maize seedlings. However, cerium addition exerted positively to relieve the damage of nitrogen metabolism process in maize seedlings caused by exposure to manganese-deficient media.

Inhibition of nitrogen and photosynthetic carbon assimilation of maize seedlings by exposure to a combination of salt stress and potassium-deficient stress.

The main aim of this work is to identify how the combined stresses affect the interdependent nitrogen and photosynthetic carbon assimilations in maize. Maize plants were cultivated in Meider's solution. They were subjected to salt stress and potassium deficiency in the K-present Meider's media and K-deficient Meider's media. After 5 weeks, we measured chlorophyll a fluorescence and the activities of several enzymes in metabolic checkpoints coordinating primary nitrogen and carbon assimilation in the leaves of maize. The study showed that the combination of salt stress and potassium-deficient stress more significantly decreased nitrate uptake, plant growth, the activities of nitrate reductase, glutamate dehydrogenase, glutamate synthase, urease, glutamic-pyruvic transaminase, glutamic-oxaloace transaminase, sucrose-phosphate synthase, phosphoenolpyruvate carboxylase, and the synthesis of free amino acids, chlorophyll, and protein than those of each individual stress, respectively. However, the combined stresses significantly increased the accumulation of ammonium and carbohydrate products. The combined stresses also significantly decreased the oxygen evolution, the electron transport, and the efficiency of photochemical energy conversion by photosystem II in maize seedlings. Taken together, a combination of salt stress and potassium-deficient stress impaired the assimilations of both nitrogen and carbon and decreased the photosystem II activity in maize.

Oxidative injury in the brain of mice caused by lanthanid.

The organ toxicity of lanthanides (Ln) on organisms had been recognized, but very little is known about the oxidative injury of brain caused by Ln. In order to study the mechanisms underlying the effects of Ln on the brain, ICR mice were injected with a single 20 mg/kg body weight dose of LaCl(3), CeCl(3), and NdCl(3) into the abdominal cavity daily for 14 days. We then examined the coefficient of the brain, the brain pathological changes and oxidative stress-mediated responses, and the accumulation of Ln and levels of neurochemicals in the brain. The results showed that CeCl(3) and NdCl(3) could induce some neurons to turn inflammatory cells and slight edema but did not observe the brain pathological changes from LaCl(3)-treated group. The concentrations of La, Ce, and Nd in the brain were significantly different and ranked in the order of Ce, Nd, and La. The injury of the brain and oxidative stress occurred as Ln appeared to trigger a cascade of reactions such as lipid peroxidation, the decreases of the total antioxidation capacity and activities of antioxidative enzymes, the excessive release of nitric oxide, the increase of glutamic acid, and the downregulated level of acetylcholinesterase activities. Furthermore, both Ce(3+) and Nd(3+) exhibited higher oxidative stress and toxicity on brain than La(3+), and Ce(3+) caused more severe brain injuries and oxidative stress than Nd(3+), implying that the differences in the brain injuries caused by Ln might be related to the number of 4f electrons of Ln.

Cerium relieves the inhibition of photosynthesis of maize caused by manganese deficiency.

It had been proved that manganese (Mn) deficiency could damage the photosynthesis of plants, and lanthanides could improve photosynthesis and greatly promote plant growth. However, the mechanisms on how Mn deficiency and cerium (Ce) addition affects the photosynthetic carbon reaction of plants under manganese deficiency are still poorly understood. In this study, the main aim was to determine Mn deficiency and cerium addition effects in key enzymes of CO(2) assimilation of maize. Maize plants were cultivated in Hoagland's solution. They were subjected to Mn deficiency and to Ce administered in the Mn-present Hoagland's media and Mn-deficient Hoagland's media. The growth condition, chlorophyll synthesis, and oxygen evolution were significantly destroyed by manganese deficiency, the activities of ribulose-1, 5-bisphosphate caroxylase/oxygenase (Rubisco), and Rubisco activase, and their genes expressions were inhibited by Mn deficiency. However, Ce treatment promoted the chlorophyll synthesis, oxygen evolution, and the activities of two key enzymes in CO(2) assimilation. Reverse transcription polymerase chain reaction was carried out, and the results showed that the mRNA expressions of Rubisco small subunit (rbcS), Rubisco large subunit (rbcL), and Rubisco activase subunit (rca) in the cerium-treated maize were obviously increased. One of the possible mechanisms of carbon reaction promoted by Ce is that the Ce treatment resulted in the enhancements of Rubisco and Rubisco activase mRNA amounts, the protein levels, and activities of Rubisco and Rubisco activase, thereby leading to the high rate of photosynthetic carbon reaction and enhancement of maize growth under Mn-deficient conditions. Together, the experimental study implied that Ce could partly substitute for magnesium and increase the oxidative stress-resistance of spinach chloroplast grown in Mn-deficiency conditions, but the mechanisms need further study.

Oxidative stress in the liver of mice caused by intraperitoneal injection with lanthanoides.

In order to study the mechanisms underlying the effects of lanthanoid (Ln) on the liver, ICR mice were injected with LaCl3, CeCl3, and NdCl3 at a dose of 20 mg/kg BW into the abdominal cavity daily for 14 days. We then examined oxidative stress-mediated responses in the liver. The increase of lipid peroxide in the liver produced by Ln suggested an oxidative attack that was activated by a reduction of antioxidative defense mechanisms as measured by analyzing the activities of superoxide dismutase, catalase, and ascorbate peroxidase, as well as antioxidant levels such as glutathione and ascorbic acid, which were greatest in Ce(3+) treatment, medium in Nd(3+), and least in La(3+). Our results also implied that the oxidative stress in the liver caused by Ln likely is Ce(3+) > Nd(3+) >La(3+), but the mechanisms need to be further studied in future.

Influence of lanthanides on the antioxidative defense system in maize seedlings under cold stress.

The influence of LaCl(3), CeCl(3), and NdCl(3) on the antioxidative defense system in maize seedlings under cold stress was investigated. It was found that maize seedlings cultivated in cold stress developed distinct cold symptoms, and the plant growth was significantly inhibited as expected, while Ln-treated seedling growth was improved. Cold stress in maize seedlings also increased the permeability of plasma membrane, malondialdehyde as a degradation product of lipid peroxidation, and reactive oxygen species such as superoxide radicals and hydrogen peroxide, and decreased activities of the antioxidant enzymes such as superoxide dismutase, catalase, ascorbate peroxidase, and glutathione content; however, Ln treatments cultivated in cold stress decreased the permeability of plasma membrane, malondialdehyde, and reactive oxygen species, and increased activities of the antioxidative defense system. It implied that Ln could increase oxidative-stress resistance under cold stress. On the other hand, the assay of physiological and biochemical parameters demonstrated that Ce relieving chilling injury of maize seedlings caused by cold stress was most significant, medium in the Nd treatment, and last in the La treatment. These results suggested that the increase of cold resistance of maize seedlings caused by Ln might be closely related to its properties of 4f electron shell and variable valence.

Improvement of cerium of photosynthesis functions of maize under magnesium deficiency.

Rare earth elements can promote photosynthesis, but their mechanisms are still poorly understood under magnesium deficiency. The present study was designed to determine the role of cerium in magnesium-deficient maize plants. Maize was cultivated in Hoagland's solution added with cerium with and without adequate quantities of magnesium. Under magnesium-deficient conditions, cerium can prevents inhibition of synthesis of photosynthetic pigment, improves light energy absorption and conversion, oxygen evolution, and the activity of photo-phosphorelation and its coupling factor Ca(2+)-ATPase. These results suggest that cerium could partly substitute magnesium, improving photosynthesis and plant growth.

Signaling pathway of inflammatory responses in the mouse liver caused by TiO2 nanoparticles.

In an effort to examine signaling pathway of inflammation of the mouse liver caused by intragastric administration of titanium dioxide nanoparticles (NPs), we assessed Toll-like receptor-2 (TLR2), TLR-4, IκB kinase (IKK-α, IKK-ß), IκB nucleic factor-κB (NF-κB), NF-κBP52, NF-κBP65, tumor necrosis factor-α (TNF-α), NF-κB-inducible kinase (NIK), interleukin-2 (IL-2), biochemical parameters of liver functions, and histopathological changes and liver ultrastructure in the TiO(2) NPs-treated mice. The results showed the titanium accumulation in liver, histopathological changes and hepatocytes apoptosis of mice liver, and the liver function damaged by TiO(2) NPs. The real-time quantitative reverse transcriptase polymerase chain reaction and enzyme-linked immunosorbent assay analyses showed that TiO(2) NPs can significantly increase the mRNA and protein expression of TLR2 and TLR4 and several inflammatory cytokines, including IKK1, IKK2, NF-κB, NF-κBP52, NF-κBP65, TNF-α, and NIK, and TiO(2) NPs can significantly decrease the mRNA and protein expression of IκB and IL-2. The results of this study added to our understanding of TiO(2) NPs-induced liver toxicity. It implied that the signaling pathway of liver injury in the TiO(2) NPs-stimulated mouse liver sequentially might occur via activation of TLRs→NIK→IκB kinase→NF-κB→TNF-α→inflammation→apoptosis→liver injury.

Cerium relieves the inhibition of chlorophyll biosynthesis of maize caused by magnesium deficiency.

Lanthanoids (Ln) were demonstrated to improve chlorophyll formation and the growth of plants. But the mechanism of the fact that Ln promotes chlorophyll biosynthesis of plants is poorly understood. The main aim of the study was to determine Ln effects in chlorophyll formation of maize under magnesium (Mg) deficiency. Maize plants were cultivated in Hoagland's solution. They were subjected to Mg deficiency and to cerium administered in Mg-deficient Hoagland's media, and then the contents of various chlorophyll precursors and gen expressions of the key enzymes of chlorophyll biosynthesis were examined. The decrease of chlorophyll contents in maize leaves caused by Mg deficiency suggested an inhibition of chlorophyll synthesis that was inhibited by a reduction of the precursors as measured by analyzing the contents of δ-aminolevulinic acid, porphobilinogen, uroporphyrinogen III, Mg-protoporphyrin IX, and protochlorophyll, as well as the expression levels of magnesium chelatase, magnesium-protoporphyrin IX methyltransferase, and chlorophyll synthase; Mg deficiency significantly inhibited the transformation from coproporphyrinogen III or protoporphyrin IX to chlorophyll. However, cerium addition significantly relieved the inhibition of chlorophyll biosynthesis in maize caused by Mg deficiency and increased chlorophyll content and promoted a series of transformations from δ-aminolevulinic acid to chlorophyll and maize growth under Mg deficiency. It implied that cerium might partly substitute for the role of Mg.

Neurotoxicological effects and the impairment of spatial recognition memory in mice caused by exposure to TiO2 nanoparticles.

Titanium dioxide nanoparticles (TiO(2) NPs) are now in daily use including popular sunscreens, toothpastes, and cosmetics. However, the effects of TiO(2) NPs on human body, especially on the central nervous system, are still unclear. The aim of this study was to determine whether TiO(2) NPs exposure results in persistent alternations in nervous system function. ICR mice were exposed to TiO(2) NPs through intragastric administration at 0, 5, 10 and 50 mg/kg body weight every day for 60 days. The Y-maze test showed that TiO(2) NPs exposure could significantly impair the behaviors of spatial recognition memory. To fully investigate the neurotoxicological consequence of TiO(2) NPs exposure, brain elements and neurochemicals were also investigated. The contents of Ca, Mg, Na, K, Fe and Zn in brain were significantly altered after TiO(2) NPs exposure. Moreover, TiO(2) NPs significantly inhibited the activities of Na(+)/K(+)-ATPase, Ca(2+)-ATPase, Ca(2+)/Mg(2+)-ATPase, acetylcholine esterase, and nitric oxide synthase; the function of the central cholinergic system was also noticeably disturbed and the contents of some monoamines neurotransmitters such as norepinephrine, dopamine and its metabolite 3, 4-dihydroxyphenylacetic acid, 5-hydroxytryptamine and its metabolite 5-hydroxyindoleacetic acid were significantly decreased, while the contents of acetylcholine, glutamate, and nitric oxide were significantly increased. These first findings indicated that exposure to TiO(2) NPs could possibly impair the spatial recognition memory ability, and this deficit may be possibly attributed to the disturbance of the homeostasis of trace elements, enzymes and neurotransmitter systems in the mouse brain. Therefore, the application of TiO(2) NPs and exposure effects especially on human brain for long-term and low-dose treatment should be cautious.

Hepatocyte apoptosis and its molecular mechanisms in mice caused by titanium dioxide nanoparticles.

While the hepatocyte apoptosis induced by TiO(2) nanoparticles (NPs) has been demonstrated, very little is known about the molecular mechanisms underlying this mouse liver apoptosis. In order to understand the hepatocyte apoptosis induced by intragastric administration of TiO(2) NPs for consecutive 60 days, the hepatocyte apoptosis, various oxidative stress parameters and the stress-related gene expression levels were assayed for the mouse liver. 60 days of TiO(2) NPs exposure, hepatocyte apoptosis in the liver could be observed, which was followed by increased reactive oxygen species accumulation, and decreased the stress-related gene expression levels of superoxide dismutase, catalase, glutathione peroxidase, metallothionein, heat shock protein 70, glutathione S transferase, P53, and transferrin; and the significant enhancement of the cytochrome p450 1A expression level. It implied that hepatocyte apoptosis, oxidative stresses, and alteration of expression levels of the genes related with TiO(2) NPs detoxification/metabolism regulation and radical scavenging action. Therefore, the application of TiO(2) NPs and exposure effects especially on human liver for long-term and low-dose treatment should be cautious.

Effects of manganese deficiency on spectral characteristics and oxygen evolution in maize chloroplasts.

The effects of Mn(2+) deficiency on light absorption, transmission, and oxygen evolution of maize chloroplasts were investigated by spectral methods. Several effects of Mn(2+) deficiency were observed: (1) the skeleton of pigment protein complexes and oxygen-evolving center and the combination between pigment and protein were damaged; (2) the light absorption of chloroplasts was obviously decreased; (3) the energy transfer among amino acids within PS II protein-pigment complex and decreased energy transport from tyrosine residue to chlorophyll a and from chlorophyll b and carotenoid to chlorophyll a were inhibited; (4) the oxygen-evolving of chloroplast was significantly inhibited. However, Mn(2+) addition decreased the damage of light absorption, transmission, and oxygen evolution of maize chloroplasts caused by Mn(2+) deficiency.