Heat-induced Oxidative Stress Research Articles

Brown seaweed- (Tasco) treated conserved forage enhances antioxidant status and immune function in heat-stressed wether lambs.

Twenty-seven wether lambs were utilized to evaluate select innate immunity and oxidative stress in response to diet and heat stress. Dietary treatments were: (i) control (tall fescue) hay = no Tasco (tradename for the extract of the brown seaweed, Ascophyllum nodosum, Acadian Sealants Ltd, Nova Scotia, Canada); (ii) pre-harvest Tasco-Forage-treated hay and (iii) control hay + post-harvest Tasco-EX. Tasco-Forage and Tasco-EX are two forms of the Tasco extract that are either applied to foliage or used for direct feeding, respectively. All lambs were supplemented with soyabean meal and trace mineralized salt. Heat stress was applied for 10 days with measurements obtained at days 0, 4 and 10. A heat x treatment interaction indicated hay with Tasco enhanced monocyte oxidative burst through short duration (p < 0.05) and long duration (p < 0.10) heat stress. Phagocytic activity was influenced by days of heat stress (p < 0.001) and treatment (p = 0.02) with post-harvest Tasco lambs exhibiting the greatest immune enhancement (p < 0.05). Red and white blood cell glutathione peroxidase increased by heat stress day 10 in Tasco lambs. Superoxide dismutase activity was increased and lipid hydroperoxide metabolites minimized (p < 0.01) through long duration heat stress in the pre-harvest Tasco group. Tasco treatment of tall fescue hay prior to harvest appears to provide residual effects on animal antioxidant availability in short-duration heat stress. Tasco supplementation to post-harvest fescue hay enhances immune function and protects against prolonged heat-induced oxidative stress.

Ascorbic acid and melatonin reduce heat-induced performance inhibition and oxidative stress in Japanese quails

1. The effects of ascorbic acid (l-ascorbic acid) and melatonin supplementation on performance, carcase characteristics, malondialdehyde (MDA) as lipid peroxidation indicator, ascorbic acid, retinol, tocopherol and mineral status in the Japanese quail (Coturnix coturnix japonica) exposed to high ambient temperature were evaluated. 2. Two hundred and forty Japanese quails (10 d old) were randomly assigned to 8 treatment groups consisting of 10 replicates of three birds each. The birds were kept in a temperature-controlled room at 22°C (Thermoneutral, TN groups) or 34°C (for 8 h/d; 09:00 to 17:00 h; Heat stress, HS groups). Birds in both TN and HS were fed either a basal (control) diet or the basal diet supplemented with 250 mg of l-ascorbic acid/kg of diet (Ascorbic acid group), 40 mg of melatonin/kg of diet (Melatonin group) or both (Ascorbic acid + Melatonin group). 3. Supplementing heat-stressed quails with ascorbic acid and melatonin improved performance compared with the control group. Effects generally were greatest in quails supplemented with both ascorbic acid and melatonin. 4. Although supplementation did not consistently restore the concentrations of serum ascorbic acid, retinol and tocopherol to those of TN groups, these concentrations increased significantly with supplementation. Furthermore, serum and liver MDA and serum cholesterol and glucose concentrations were lower in the supplemented groups than in the heat-stressed controls. 5. Within each environment, excretion of Ca, P, Mg, Zn, Fe and Cr were lowest in the combination group and, in all cases, highest in the HS group. Interactions between diet and temperature were detected for live weight gain, cold carcase weight, MDA, ascorbic acid, tocopherol concentrations and excretion of zinc. 6. The results of the study indicate that ascorbic acid and melatonin supplementation attenuate the decline in performance and antioxidant and mineral status caused by heat stress and such supplementation may offer protection against heat-stress-related depression in performance of Japanese quails.

Response of genes associated with mitochondrial function to mild heat stress in yeast Saccharomyces cerevisiae.

The genome-wide expression pattern of budding yeast Saccharomyces cerevisiae in response to mild heat treatment in a non-fermentable carbon source was analyzed using DNA microarrays. Of 5,870 open reading frames (nuclear genome transcripts) examined, 104 genes were upregulated and 287 genes were downregulated upon shifting of the cells from 25 degrees C to 37 degrees C. Forty upregulated genes and 235 downregulated genes encoded localization-assigned proteins. Of 113 heat-repressible genes (excluding 122 heat-repressible ribosomal genes), 36 were mitochondria-related genes, whereas only 2 of 40 heat-inducible genes were mitochondria-related. In particular, 9 genes involved in the mitochondrial respiratory chain and 7 genes involved in mitochondrial protein translocation were significantly repressed, suggesting that mitochondrial respiratory function and biogenesis were downregulated. Consistent with these findings, the growth of yeast cells in a non-fermentable carbon source was repressed at 37 degrees C and the mitochondria isolated from heat-stressed cells exhibited compromised preprotein-import activity compared with those from unstressed cells. In contrast, many genes involved in glycolysis and the metabolic pathway to produce glutamate via the tricarboxylic acid cycle, which is essential for biosynthetic reactions, were upregulated. Yeast cells might downregulate mitochondrial function to circumvent heat-induced oxidative stress, upregulate stress-related genes, and remodel genes for metabolic pathways in response to mild heat stress: an adaptive response at the expense of cell growth.

Mitochondrial respiratory electron carriers are involved in oxidative stress during heat stress in Saccharomyces cerevisiae.

In the present study we sought to determine the source of heat-induced oxidative stress. We investigated the involvement of mitochondrial respiratory electron transport in post-diauxic-phase cells under conditions of lethal heat shock. Petite cells were thermosensitive, had increased nuclear mutation frequencies, and experienced elevated levels of oxidation of an intracellular probe following exposure to a temperature of 50 degrees C. Cells with a deletion in COQ7 leading to a deficiency in coenzyme Q had a much more severe thermosensitivity phenotype for these oxidative endpoints following heat stress compared to that of petite cells. In contrast, deletion of the external NADH dehydrogenases NDE1 and NDE2, which feed electrons from NADH into the electron transport chain, abrogated the levels of heat-induced intracellular fluorescence and nuclear mutation frequency. Mitochondria isolated from COQ7-deficient cells secreted more than 30 times as much H(2)O(2) at 42 as at 30 degrees C, while mitochondria isolated from cells simultaneously deficient in NDE1 and NDE2 secreted no H(2)O(2). We conclude that heat stress causes nuclear mutations via oxidative stress originating from the respiratory electron transport chains of mitochondria.