Effect of light emitted by diodes on growth and pigment content of black currant plantlets in vitro

The effects of cool white, natural white, and warm white lights, which have a continuous spectrum throughout the region of surfactant, and blue-red light spectrum on in vitro growth and development of black currant (Ribes nigrum L.) was studied. It was demonstrated that the spectral composition of light affected length and fresh mass of shoots and roots as well as concentrations of chlorophylls, carotenoids, and anthocyanins. The plants grown under warm white light had the longest shoots (2.5 ± 0.2 cm) and fresh mass of shoots (166 ± 12 mg) and roots (80 ± 16 mg) relatively to оne’s grown under other light types. Under blue-red and warm white lights black currant leaves possessed the highest concentrations of chlorophyll a (2.66 ± 0.31 and 2.17 ± 0.14 µmol·gwm-1, respectively), chlorophyll b (1.15 ± 0.15 and 0.87± 0.05 µmol·gwm-1), carotenoids (0.89 ± 0.09 and 0.78 ± 0.05 µmol·gwm-1, respectively) and anthocyanins (1.37 ± 0.20 and 1.09 ± 0.05 µmol·gwm-1, respectively). Thus, blue-red (B:R = 1:4) and warm white lights may be used as an alternative light source for upland black currant culture systems

Pesticide toxicity

Pesticides are known for their high persistence and pervasiveness in the environment, and along with products of their biotransformation, they may remain in and interact with the environment and living organisms in multiple ways, according to their nature and chemical structure, dose and targets. In this review, the classifications of pesticides based on their nature, use, physical state, pathophysiological effects, and sources are discussed. The effects of these xenobiotics on the environment, their biotransformation in terms of bioaccumulation are highlighted with special focus on the molecular mechanisms deciphered to date. Basing on targeted organisms, most pesticides are classified as herbicides, fungicides, and insecticides. Herbicides are known as growth regulators, seedling growth inhibitors, photosynthesis inhibitors, inhibitors of amino acid and lipid biosynthesis, cell membrane disrupters, and pigment biosynthesis inhibitors, whereas fungicides include inhibitors of ergosterol biosynthesis, protein biosynthesis, and mitochondrial respiration. Insecticides mainly affect nerves and muscle, growth and development, and energy production. Studying the impact of pesticides and other related chemicals is of great interest to animal and human health risk assessment processes since potentially everyone can be exposed to these compounds which may cause many diseases, including metabolic syndrome, malnutrition, atherosclerosis, inflammation, pathogen invasion, nerve injury, and susceptibility to infectious diseases. Future studies should be directed to investigate influence of long term effects of low pesticide doses and to minimize or eliminate influence of pesticides on non-target living organisms, produce more specific pesticides and using modern technologies to decrease contamination of food and other goods by pesticides

Goldfish brain and heart are well protected from Ni2+-induced oxidative stress

After 96 h goldfish exposure to 10, 25 or 50 mg/L of Ni2 + no Ni accumulation was found in the brain, but lipid peroxide concentration was by 44% elevated in the brain, whereas carbonyl protein content was by 45–45% decreased in the heart. High molecular mass thiol concentration was enhanced by 30% in the heart, while in the brain low molecular mass thiol concentration increased by 28–88%. Superoxide dismutase activity was by 27% and 35% increased in the brain and heart, respectively. Glutathione peroxidase activity was lowered to 38% and 62% of control values in both tissues, whereas catalase activity was increased in the heart by 15–45%, accompanied by 18–29% decreased glutathione reductase activity. The disturbances of free radical processes in the brain and heart might result from Ni-induced injuries to other organs with more prominent changes in the heart, because of close contact of this organ with blood, whereas the blood–brain barrier seems to protect the brain

Tissue-specific induction of oxidative stress in goldfish by 2,4-dichlorophenoxyacetic acid: Mild in brain and moderate in liver and kidney

This study investigated the effects of the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) on free radical-related processes in tissues of goldfish given 96. h exposures to 1, 10 or 100. mg/L of 2,4-D as well as 96. h recovery from the 100. mg/L treatment. In liver, 2,4-D exposure increased levels of protein carbonyls and lipid peroxides by 36-53% and 24-43%, respectively, but both parameters reverted during recovery, whereas in brain glutathione status improved in response to 2,4-D. Lipid peroxide content in kidney was enhanced by 40-43% after exposure to 2,4-D with a decrease during recovery. Exposure to 2,4-D also reduced liver acetylcholinesterase activity by 31-41%. The treatment increased catalase activity in brain, but returned it to initial levels after recovery. In kidney, exposure to 100. mg/L of 2,4-D caused a 33% decrease of superoxide dismutase activity. Thus, goldfish exposure to 2,4-D induced moderate oxidative stress in liver and kidney and mild oxidative stress in brain

Effect of prometryn-containing herbicide gesagard on hematological profiles and biochemical parameters in goldfish liver and plasma

The impact of goldfish exposure for 96 h to herbicide Gesagard 500 FW at concentrations 0.2, 1, or 5 mg L−1 (corresponding to 0.1, 0.5 or 2.5 mg L-1 of effective compound prometryn) on the hematological profile of blood and biochemical parameters of plasma and liver was studied. Fish exposure to low concentration of the herbicide (0.2 mg L-1) slightly decreased liver glycogen and plasma lactate levels. Plasma glucose levels rose by 27% in goldfish exposed to 1 mg L-1 Gesagard. The activity of lactate dehydrogenase decreased by 63% and 36% in plasma of fish exposed to herbicide at concentrations 1 and 5 mg L-1, respectively, but was not affected in liver. Goldfish exposure to the highest concentration of Gesagard (5 mg L-1) decreased hematocrit by 23% and increased monocyte count by 57%, and elevated triacylglycerol level by 91% in plasma. Overall, the results indicate that acute exposure to Gesagard induced minor changes in the hematological and biochemical parameters of goldfish, suggesting that disruptions of these parameters may provide early warning signs that could be useful for assessing acute or sublethal toxic effects of pesticides on aquatic species

Oxidative stress responses in gills of goldfish, Carassius auratus, exposed to the metribuzin-containing herbicide Sencor

Metribuzin belongs to the family of asymmetrical triazine compounds and is an active ingredient in many commercial herbicides including Sencor. Effects on goldfish (Carassius auratus L.) of exposure for 96 h to 7.14, 35.7 or 71.4 mg L-1 Sencor 70 WG (corresponding to 5, 25 and 50 mg L-1 of metribuzin) were examined by evaluating oxidative stress markers and activities of antioxidant and associated enzymes in gills. Fish exposed to the lowest Sencor concentration (7.14 mg L-1) showed a 94% increase in levels of protein carbonyls in gills as well as 45% and 144% increases in the activities of glutathione peroxidase and glutathione-S-transferase. Exposure to the highest Sencor concentration (71.4 mg L-1) resulted in reduced levels of protein carbonyls by 56% and lipid peroxides by 40%, as compared with controls, but enhanced levels of low and high molecular mass thiols by 71% and 36%, respectively. The activities of superoxide dismutase, glutathione peroxidase and glutathione-S-transferase were increased in gills of goldfish exposed to 71.4 mg L-1 Sencor. At any concentration tested, Sencor did not affect the activities of glutathione reductase, glucose-6-phosphate dehydrogenase, lactate dehydrogenase or acetylcholine esterase in gills. The results of this study indicate that acute exposure of goldfish to Sencor had effect on free radical processes in gills and glutathione-dependent antioxidants effectively protect proteins and lipids from oxidation