Response of nitrogen metabolism to boron toxicity in tomato plants

Boron (B) toxicity has become important in areas close to the Mediterranean Sea where intensive agriculture has been developed. The objective of this research was to study the effects of B toxicity (0.5 m m and 2.0 m m B) on nitrogen (N) assimilation of two tomato cultivars that are often used in these areas. Leaf biomass, relative leaf growth rate (RGR_L), concentration of B, nitrate (NO₃⁻), ammonium (NH₄⁺), organic N, amino acids and soluble proteins, as well as nitrate reductase (NR), nitrite reductase (NiR), glutamine synthase (GS), glutamate synthetase (GOGAT) and glutamate dehydrogenase (GDH) activities were analysed in leaves. Boron toxicity significantly decreased leaf biomass, RGR_L, organic N, soluble proteins, and NR and NiR activities. The lowest NO₃⁻ and NH₄⁺ concentration in leaves was recorded when plants were supplied with 2.0 m m B in the root medium. Total B, amino acids, activities of GS, GOGAT and GDH increased under B toxicity. Data from the present study prove that B toxicity causes inhibition of NO₃⁻ reduction and increases NH₄⁺ assimilation in tomato plants.     

In vitro analysis of intestinal absorption of cadmium and calcium in rainbow trout fed with calcium- and cadmium-supplemented diets

The protective effects of dietary Ca²⁺ supplementation against Cd accumulation in rainbow trout Oncorhynchus mykiss fed with Cd-contaminated food were evaluated in relation to chronic changes in intestinal absorption rates. The changes were measured ' in vitro '. The control diet contained c. 20 mg Ca²⁺ g⁻¹ food and 0·25 μg Cd g⁻¹ food; the experimental diets were supplemented with CaCO₃ and Cd(NO₃)₂·4H₂O to levels of 50 mg Ca²⁺ g⁻¹ food and 300 μg Cd g⁻¹ food, alone and in combination. The Ca²⁺ and Cd absorption rates were measured using radiotracers (⁴⁵Ca, ¹⁰⁹Cd) at total Ca²⁺ and Cd concentrations of 3·0 and 0·12 mmol l⁻¹, respectively in the intestinal saline. Chronically elevated dietary Cd caused a significant increase in Cd absorption rate by up to 10-fold at 30 days in the mid-intestine. The high Ca²⁺ diet prevented this up-regulation of Cd transport rate. Conversely, intestinal Ca²⁺ absorption was significantly increased by two- to five-fold by the Ca²⁺-supplemented diet at 30 days in both the mid- and posterior intestine, and this effect was eliminated when Cd was simultaneously elevated in the diet. Ca²⁺ and Cd probably interact at common pathways and transport mechanisms in the intestine, though independent pathways may also exist.     

Further Observations on the Toxicity of Navy Beans (Phaseolus vulgaris) for Japanese Quail (Coturnix coturnix japonica)

S ummary . The lethal and growth depressing effects of feeding raw navy beans (RNB) to Japanese quail have been shown to be due neither to poor palatability nor to dialysable, lipid or carbohydrate constituents, but to a protein material soluble at pH 3 and precipitable by saturation with (NH₄)₂SO₄. This material proved resistant to digestion by pepsin and proteolytic bacteria but was destroyed by autoclaving at 121° for 15 min. Germfree birds given a diet containing RNB which had been fermented by coliforms grew well, indicating that toxicity of RNB is not dependent on the release by intestinal bacteria of poisons from innocuous precursors in the beans. Examination of the effects of feeding diets containing other raw legume seeds to quail have shown that toxicity is associated with the presence of high concentrations of phytohaemagglutinins (PHAs). Quail given RNB diet showed a greater incidence of liver infection than birds fed an autoclaved bean diet but bacteriological examination of gut contents of such birds revealed no marked qualitative or quantitative differences. Chemical examination of gut contents likewise revealed no marked differences. Experiments with gnotobiotic quail showed that coliforms derived from a variety of sources were capable of causing the death of birds on RNB diet and that the numbers attained in different parts of the intestine by a single coliform strain were not affected by the diet fed. The results suggest that toxicity of RNB may be due to impairment of body defence mechanisms by PHA leading to tissue invasion by normally innocuous components of the intestinal microflora.     

Morphological and functional alterations induced in trout intestine by dietary cadmium and lead

Effects of oral administration of lead and cadmium on structure and function of trout intestine were investigated in Salmo gairdneri. Fish were fed either cadmium (5 mg kg*¹ fish per day) or lead (10 mg kg⁻¹ fish p er day) and sacrificed after a 15 or 30 day treatment.
Levels of cadmium and lead in kidney, liver and spleen were significantly increased by the 15th day of treatment.
Following both cadmium and lead treatment, morphological observations showed an increased mucous cell activity, a disruption of intestinal brush border and an increased renewal rate of absorptive cells.
Influx (J_ms), outflux (J_sm) of chlorine and sodium ion and net fluxes were measured on perfused intestinal segments and ouabain-sensitive sodium, potassium-ATPase (Na, K-ATPase) activity was determined on intestinal scrapings. Cadmium did not alter either sodium chlorine transepithelial fluxes or sodium, potassium-ATPase activity, but lead did. In the middle intestine, lead modified significantly transepithelial sodium and chlorine fluxes (J_ms Na: 3.21 ± 0.34 to 1.79 ± 0.29 and J_ms Cl: 3.32 ± 0.34 to 1.86 ± 0.22μmol h⁻¹ cm⁻², n = 6) after 30-day diet. J_net remain unchanged and Na, K-ATPase activity decreased. In the posterior intestine, lead altered only J_ms Na (1.95 ± 0.31 to 0.37 ± 0.09μmol h⁻¹ cm⁻²) and J_ms Cl. Consequently J_nes were also decreased.
So, although both cadmium and lead induce morphological disorders in the middle and in the posterior intestine of the trout, they have different effects on the absorption mechanisms of ions.     

The Desglycinyl Metabolite of Remacemide Hydrochloride Is Neuroprotective in Cultured Rat Cortical Neurons

Abstract: The neuroprotective actions of remacemide and its anticonvulsant metabolite 1,2-diphenyl-2-propylamine monohydrochloride (desglycinylremacemide; DGR), a low-affinity NMDA receptor antagonist, were investigated using primary rat cortical neuronal cultures. Exposure of cortical cultures to NMDA (100 µ M ) for 15 min killed 85% of the neurons during the next 24 h. This neurotoxicity was blocked in a concentration-dependent manner by adding DGR (5–20 µ M ), but not its remacemide precursor (10–100 µ M ), to the cultures during the time of NMDA exposure. This suggests that the neuroprotective, as well as the anticonvulsant, activity of remacemide is mediated by DGR. Neuroprotective concentrations of DGR also inhibited two of the principal acute effects of NMDA. DGR (5–20 µ M ) prevented the loss of membrane-associated protein kinase C (PKC) activity that developed by 4 h after transient exposure to 100 µ M NMDA and reduced the NMDA-triggered increases in intracellular free Ca²⁺ concentration ([Ca²⁺]_i) by up to 70%. By contrast, remacemide (50 and 100 µ M ) did not prevent the NMDA-induced loss of PKC activity or reduce the [Ca²⁺]_i responses. These data suggest that DGR protection against NMDA-mediated toxicity in cultured cortical neurons is associated with a reduction of NMDA-triggered [Ca²⁺]_i surges and a prevention of the loss of membrane-associated PKC activity. In addition, the inhibition of NMDA-triggered [Ca²⁺]_i responses by DGR was qualitatively different from the inhibition of these responses by the high-affinity NMDA-receptor antagonists MK-801 and phencyclidine. This may be a consequence of DGR's lower affinity for the NMDA receptor.     

Cytochalasins Protect Hippocampal Neurons Against Amyloid β-Peptide Toxicity: Evidence that Actin Depolymerization Suppresses Ca2+ Influx

Abstract: Increasing data suggest that the amyloid β-peptide (Aβ), which accumulates in the brains of Alzheimer's victims, plays a role in promoting neuronal degeneration. Cell culture studies have shown that Aβ can be neurotoxic and recent findings suggest that the mechanism involves destabilization of cellular calcium homeostasis. We now report that cytochalasin D, a compound that depolymerizes actin microfilaments selectively, protects cultured rat hippocampal neurons against Aβ neurotoxicity. Cytochalasin D was effective at concentrations that depolymerized actin (10–100 n M ). The elevation of [Ca²⁺]_i induced by Aβ, and the enhancement of [Ca²⁺]_i responses to glutamate in neurons exposed to Aβ, were markedly attenuated in neurons pretreated with cytochalasin D. The protective effect of cytochalasin D appeared to result from a specific effect on actin filaments and reduction in calcium influx, because cytochalasin E, another actin filament-disrupting agent, also protected neurons against Aβ toxicity; the microtubule-disrupting agent colchicine was ineffective; cytochalasin D did not protect neurons against the toxicity of hydrogen peroxide. These findings suggest that actin filaments play a role in modulating [Ca²⁺]_i responses to neurotoxic insults and that depolymerization of actin can protect neurons against insults relevant to the pathogenesis of Alzheimer's disease.     

Role of Cyclic GMP in the Regulation of Neuronal Calcium and Survival by Secreted Forms of β-Amyloid Precursor

Abstract: The Alzheimer's disease (AD) β-amyloid precursor proteins (βAPPs) are large membrane-spanning proteins that give rise to the βA4 peptide deposited in AD amyloid plaques. βAPPs can also yield soluble forms (APP^ss) that are potently neuroprotective against glucose deprivation and glutamate toxicity, perhaps through their ability to lower the intraneuronal calcium concentration ([Ca²⁺]_i). We have investigated the mechanism through which APP^ss exert these effects on cultured hippocampal neurons. The ability of APP^ss to lower rapidly [Ca²⁺]_i was mimicked by membrane-permeable analogues of cyclic AMP (cAMP) and cyclic GMP (cGMP), as well as agents that elevate endogenous levels of these cyclic nucleotides. However, only cGMP content was increased by APP^s treatment, and specific inhibition of cGMP-dependent protein kinase (but not cAMP-dependent kinase) blocked the activity of APP^ss. A membrane-permeable analogue of cGMP (8-bromo-cGMP) also mimicked the ability of APP^ss to attenuate the elevation of [Ca²⁺]_i by glutamate, apparently through inhibition of NMDA receptor activity. In addition, 8-bromo-cGMP afforded protection against glucose deprivation and glutamate toxicity, and the protection by APP^ss against glucose deprivation was blocked by an inhibitor of cGMP-dependent kinase. Together, these data suggest that APP^ss mediate their [Ca²⁺]_i-lowering and excitoprotective effects on target neurons through increases in cGMP levels.     

Fractionation of δ15N and δ13C for Atlantic salmon and its intestinal cestode Eubothrium crassum

Stable isotopes of nitrogen (δ¹⁵N) and carbon (δ¹³C) were measured for Atlantic salmon Salmo salar and their intestinal cestode, Eubothrium crassum , sharing the same diet. Atlantic salmon muscle tissues were enriched in ¹⁵N and depleted in ¹³C compared to their prey (sprat Sprattus sprattus sprattus ) and their intestinal cestode. There was no significant difference in δ¹⁵N or δ¹³C between E. crassum and the sprat. Differences in nutrient uptake and intestine physiology between Atlantic salmon and E. crassum are discussed, as well as how these may give rise to different fractionations of stable isotopes between a host and its parasites. Furthermore, Atlantic salmon contained a significantly higher lipid content than their prey, which may partly explain differences in δ¹³C values between the host and its cestode. In addition, cestodes inhabiting lipid-rich hosts were also lipid rich. Larger Atlantic salmon were enriched in ¹⁵N compared to smaller fish. Cestodes inhabiting large hosts were also enriched in ¹⁵N compared to parasites living in smaller hosts. The last two results were explained by larger fish possibly feeding from a higher trophic level, or from larger and older prey, that resulted in both a higher lipid content and an enrichment in ¹⁵N.     

Acute toxicity of copper, zinc and manganese in single and mixed salt solutions to juvenile longfin dace, Agosia chrysogaster

The acute toxicity of copper, zinc and manganese and copper-zinc and copper-manganese mixtures were determined for juvenile longfin dace, Agosia chrysogaster in hard water bioassays (mean=218 mg 1⁻¹ CaCO₃). Copper-zinc was the most lethal toxicant (96-h L.c.₅₀= 0.21 mg 1⁻¹ copper and 0.28 mg 1⁻¹ zinc) and exhibited a more than additive toxicity which was in contrast to the additive toxicity of copper-manganese mixtures (96-h L.c.₅₀= 0.45 mg 1⁻¹ copper and 64.0 mg 1⁻¹ manganese). The toxicity of copper (96-h L.c.₅₀= 0.86 mg 1⁻¹) and zinc (96-h L.c.₅₀= 0.79 mg 1⁻¹) to the fish was similar but both were considerably more lethal than manganese (96-h L.c.₅₀= 130 mg 1⁻¹).     

Abscisic acid accumulation and cadmium tolerance in rice seedlings

Rice ( Oryza sativa L.) seeds were soaked for 18 h in distilled water in the absence (–PBZ) or presence (+PBZ, a triazole) of 100 mg l⁻¹ paclobutrazol and then air dried. These air-dried seeds were germinated in the dark and then cultivated in a Phytotron. Twelve-day-old –PBZ and +PBZ seedlings were treated or not with CdCl₂. Cd toxicity was judged by the decrease in biomass production, decrease in chlorophyll and protein content, increase in NH₄⁺ content and induction of oxidative stress. The results indicated that PBZ applied to seeds was able to protect rice seedlings from Cd toxicity. On treatment with CdCl₂, the abscisic acid (ABA) content increased in +PBZ leaves, but not in –PBZ leaves. The decrease in the transpiration rate of –PBZ seedlings by CdCl₂ was less than that of +PBZ seedlings. Exogenous application of the ABA biosynthesis inhibitor, fluridone (Flu), reduced ABA accumulation, increased the transpiration rate and Cd content, and decreased the Cd tolerance of +PBZ seedlings. The effects of Flu on the Cd toxicity, transpiration rate and Cd content were reversed by the application of ABA. It seems that the PBZ-induced Cd tolerance of rice seedlings is mediated through an accumulation of ABA.     

Functional impairment of rat Kupffer cells induced by aflatoxin B1 and its metabolites

Abstract Contamination of food with mycotoxins is a major health problem. Impairment of several immune functions has been repeatedly reported in animals fed with contaminated fodder. Since the liver is a major target of toxicity by aflatoxins, the effects of aflatoxins B1, and its hepatic metabolites Q₁ and M₁ on Kupffer cell function was investigated in vitro. Aflatoxin B₁ induced significant ( P < 0.05) inhibition of phagocytosis, intracellular killing of Candida albicans , and intrinsic anti-Herpes virus activity at concentrations as low as 0.01 pg ml⁻¹. Aflatoxin Q₁ and M₁ had similar effects on phagocytosis and microbicidal activity, but were two- to ten-fold less potent than aflatoxin B₁.     

Dose responses of two pea lines to ultraviolet‐B radiation (280–315 nm)

UV‐B dose responses of two lines of pea were quantified at 2.3, 4.6, 6.9 and 9.2 kJ m⁻² day⁻¹ UV‐B (weighted according to Caldwell's generalised plant action spectrum) in controlled environments providing near‐field doses of photosynthetic radiation. Increasing UV‐B significantly increased UV‐B absorbing compounds in both lines. In the UV‐B sensitive line, JI1389, increasing UV‐B significantly inhibited most aspects of plant morphology and biomass. In the more UV‐B‐tolerant line, Scout, increasing UV‐B significantly reduced foliage area but had no effect on above‐ground biomass, although root biomass was significantly increased. Reduced plant height in JI1389 was caused by shorter internodes, in turn due to reduced cell number but not cell length. UV‐B had no significant effects on photosynthesis in either line. Significant dose responses were linear for the growth of the main stem in JI1389 but remaining significant dose responses were better fitted by quadratics with maximum UV‐B effects occurring in the range 5–7 kJ m⁻² day⁻¹ PAS300, due to stimulation of branch growth at the highest dose. However, growth stimulation by UV‐B was confined to PAS300 doses which at temperate latitudes would result only from rather extreme ozone depletions. We conclude that investigations using relatively low UV‐B doses, rather than those well above the current maximum, may be the best approach to both understanding of the fundamental mechanisms of plant responses to UV‐B and quantifying the magnitude of responses to stratospheric ozone depletion.     

Amyloid β-Mediated Oxidative and Metabolic Stress in Rat Cortical Neurons: No Direct Evidence for a Role for H2O2 Generation

Abstract: H₂O₂ and free radical-mediated oxidative stresses have been implicated in mediating amyloid β(1–40) [Aβ(1–40)] neurotoxicity to cultured neurons. In this study, we confirm that addition of the H₂O₂-scavenging enzyme catalase protects neurons in culture against Aβ-mediated toxicity; however, it does so by a mechanism that does not involve its ability to scavenge H₂O₂. Aβ-mediated elevation in intracellular H₂O₂ production is suppressed by addition of a potent H₂O₂ scavenger without any significant neuroprotection. Three intracellular biochemical markers of H₂O₂-mediated oxidative stress were unchanged by Aβ treatment: (a) glyceraldehyde-3-phosphate dehydrogenase activity, (b) hexose monophosphate shunt activity, and (c) glucose oxidation via the tricarboxylic acid cycle. Ionspray mass spectra of Aβ in the incubation medium indicated that Aβ itself is an unlikely source of reactive oxygen species. In this study we demonstrate that intracellular ATP concentration is compromised during the first 24-h exposure of neurons to Aβ. Our results challenge a pivotal role for H₂O₂ generation in mediating Aβ toxicity, and we suggest that impairment of energy homeostasis may be a more significant early factor in the neurodegenerative process.     

Flight responses of tsetse flies (Glossina) to octenol and acetone vapour in a wind-tunnel

Abstract. Female Glossina morsitans morsitans Westwood were video-recorded in a wind-tunnel as they entered, in crosswind flight, a broad plume of either octenol or acetone (two components of ox odour). Both odours produced upwind turning responses (in-flight anemotaxis) to a range of concentrations, with thresholds at around 10^-8mg1^-l for octenol and 10^-6mg1^-1 for acetone. Kinetic responses were unaffected by octenol at low concentrations, but flight speed was significantly reduced and sinuosity (^om^-1) and angular velocity (^os^-1) significantly increased by concentrations at or above those in ox breath; for acetone, these effects were apparent but inconsistently related to concentration. It is concluded that octenol and acetone vapour are used by tsetse flies to locate hosts by upwind anemotaxis, probably combined with kinetic responses. The behavioural basis for the 'repellency' of high octenol concentrations in the field is discussed in the context of the virtual loss of upwind anemotaxis to octenol at the highest concentration tested in the tunnel (30 × ox breath).     

Role of sodium in the ABA‐mediated long‐term growth response of bean to salt stress

Long‐term salt effects on plant growth have often been related to direct ion toxicity due to the accumulation of high ion concentrations in plant tissue. This work examines the relative importance of endogenous ABA, as well as Na⁺ and Cl⁻ toxicity, in the inhibition of leaf growth and photosynthesis, in bean plants grown at 1, 25, 50 and 75 m M NaCl until the fruit‐bearing stage. All salt‐treated plants showed very high leaf Cl⁻ concentrations, with little difference between plants exposed to 50 or 75 m M NaCl. The 25 and 50 mM salt‐treated plants were able to successfully exclude Na⁺ from their leaves, and only suffered an initial decline in the rate of leaf growth. Plants exposed to 75 m M NaCl showed an increase in Na⁺ leaf concentrations with an accompanying decrease in growth and photosynthesis as salt exposure progressed. A high correlation was found between leaf Na⁺ and leaf growth. Leaf ABA significantly increased with salt supply, and was highly correlated with both leaf Na⁺ and leaf growth. Our results suggest that in bean plants under long‐term salt stress, leaf ABA may participate in the regulation of leaf growth, and leaf Na⁺ would be at least partly responsible for increased ABA levels.     

A rapid assay for aluminium phytotoxicity at submicromolar concentrations

Investigations of Al phytotoxicity, including the identification of the Al species responsible for toxicity, require a rapid assay procedure employing very low concentrations of Al and a chemically simple rooting medium. Root elongation in newly germinated red clover ( Trifolium pratense L. cv. Kenland) was inhibited by submicromolar concentrations of Al. Ca²⁺ at concentrations of at least 0.2 m M was essential for optimal elongation in control seedlings. Ca²⁺ also relieved Al toxicity with the net effect that maximum reduction of elongation by 1 μ M Al was achieved at 0.2 m M Ca²⁺. Elongation in control seedlings was at least 90% of maximum from pH 4.5 to 5.7. Increases in pH relieved Al toxicity so that maximum sensitivity to 1 μ M Al occurred at pH 4.7. As a consequence of these experiments and other considerations we chose for our basic assay a medium composed of 0.2 m M CaSO₄ adjusted to pH 4.5 with H₂SO₄, variously supplemented with Al₂(SO₄)₃.
Day-old seedlings were incubated in this aerated medium in the dark at 23°C for one day. No additions of other solutes increased the sensitivity of the assay, but amelioration of Al toxicity was effected by Mg²⁺, F^-, phosphate and citrate. Increases in ionic strength per se had comparatively little effect on the toxic effects of Al. Two barley cultivars ( Hordeum vulgare L. cv. Dayton and Kearney) and two wheat cultivars ( Triticum aestivum L. cv. Hart and Thorne) known to differ in sensitivity to Al were reliably separated at submicromolar Al concentrations by the assay procedure, which was slightly modified. Suggestions for the improvement of the assay and for applications to future research are offered.     

Aluminum enhancement of plant growth in acid rooting media. A case of reciprocal alleviation of toxicity by two toxic cations

The generally rhizotoxic ion Al³⁺ often enhances root growth at low concentrations. The hypothesis that Al³⁺ enhances growth by relieving H⁺ toxicity was tested with wheat seedlings ( Triticum aestivum L.). Growth enhancement by Al³⁺ only occurred under acidic conditions that reduced root elongation. Al³⁺ increased cell membrane electrical polarity and stimulated H⁺ extrusion. Previous investigations have shown that Al³⁺ decreases solute leakage at low _pH and that the alleviation of H⁺ toxicity by cations appears to be a general phenomenon with effectiveness dependent upon charge (C³⁺>C²⁺>C^l+). Alleviation of one cation toxicity by another toxic cation appears to be reciprocal so that Al³⁺ toxicity is relieved by H⁺. It has been argued previously that this latter phenomenon accounts for the apparent toxicity of ALOH²⁺ and Al(OH)⁺₂. Reduction of cell-surface electrical potential by the ameliorative cation may reduce the cell-surface activity of the toxic cation.     

SAXITOXIN TETRODOTOXIN AND THE METABOLISM AND CATION FLUXES IN ISOLATED CEREBRAL TISSUES

Abstract— Saxitoxin and tetrodotoxin at low concentrations (10⁻⁷-10⁻⁸ M) exerted similar inhibitory effects on the increase in lactate production and the redistrjbution of Na⁺ and K⁺ that normally accompany electrical stimulation of rat cerebral cortical slices. In contrast, the toxins exerted dissimilar effects on the production of lactate in response to low concentrations of Ca²⁺ in the medium. Inhibition by tetrodotoxin occurred at a higher concentration of Ca²⁺ and was significantly greater than that produced by saxitoxin at concentrations of Ca²⁺ below 0.75 mM. These differences were not related to differential effects on the redistribution of Na⁺ and K⁺ under such conditions. The toxins had different effects on Ca²⁺ influx. Tetrodotoxin, but not saxitoxin, inhibited the influx of Ca²⁺ in the absence of electrical stimulation. The influx of Ca²⁺ increased when electrical pulses were applied and tetrodotoxin inhibited this increase, whereas saxitoxin potentiated influx of Ca²⁺ during stimulation. Our results suggest that metabolic responses to conditions that increase excitability are not governed solely by changes in the distribution of Na⁺ and K⁺. The differential effects of the toxins on Ca²⁺ fluxes suggest that one site of Ca²⁺ entry during electrical stimulation may be functionally independent of Na⁺ entry.     

Photosynthesis of two poplar clones under long‐term exposure to ozone

The photosynthetic response was studied in two clones ( Populus deltoides × maximowiczii Eridano and Populus × euramericana I‐214), known for their differential response to ozone (O₃) in terms of visible symptoms, when exposed to O₃ (60 nl l⁻¹ 5 h day⁻¹, 7 and 15 days). The photosynthetic ability was tested using gas exchange and chlorophyll fluorescence analysis. O₃ caused a decrease in the CO₂ assimilation rate at light saturation level in mature leaves of both clones. Alterations of Chl fluorescence parameters, in particular the F_v/F_m ratio and non‐photochemical quenching were also observed. The effects were similar for both clones and it could not be concluded that differential effects on electron transport capacity were responsible for the observed reduction in photosynthesis. The reduction of photosynthetic rate in Eridano was due mainly to a reduced mesophyll activity, as evidenced by the increase in intercellular CO₂ concentration and the minimal changes in stomatal conductance. In contrast, in I‐214, stomatal effects were primarily responsible, although effects on the mesophyll cannot be excluded. Data obtained indicate that the effects observed at the mesophyll level may be attributed to indirect effects caused by membrane disorders.     

Cadmium toxicity to rainbow trout, Salmo gairdneri Richardson: a study of eggs and alevins

Cadmium toxicity to rainbow trout was evaluated at two cadmium concentrations (0.01, 0.10 mg1⁻¹) and in water without added cadmium using eggs reared through the larval (alevin) phase to swim-up fry. Exposure to 0.1 mg Cd 1⁻¹ promoted premature hatching, retarded growth, increased rates of mortality and the occurrence of developmental abnormalities such as spinal curvature and blood clots. Three methods of holding the eggs and alevins during the toxicity test were compared. Hatching time and success, alevin mortality, growth and development were not influenced by the method of containment but of the three methods, a subdivided perforated box system proved particularly useful for monitoring the responses of specific animals throughout the toxicity test.