Repetitive Heat Stress Research Articles

Structural and Functional Heat Stress Responses of Chloroplasts of Arabidopsis thaliana.

Temperature elevations constitute a major threat to plant performance. In recent years, much was learned about the general molecular mode of heat stress reaction of plants. The current research focuses on the integration of the knowledge into more global networks, including the reactions of cellular compartments. For instance, chloroplast function is central for plant growth and survival, and the performance of chloroplasts is tightly linked to the general status of the cell and vice versa. We examined the changes in photosynthesis, chloroplast morphology and proteomic composition posed in Arabidopsis thaliana chloroplasts after a single or repetitive heat stress treatment over a period of two weeks. We observed that the acclimation is potent in the case of repetitive application of heat stress, while a single stress results in lasting alterations. Moreover, the physiological capacity and its adjustment are dependent on the efficiency of the protein translocation process as judged from the analysis of mutants of the two receptor units of the chloroplast translocon, TOC64, and TOC33. In response to repetitive heat stress, plants without TOC33 accumulate Hsp70 proteins and plants without TOC64 have a higher content of proteins involved in thylakoid structure determination when compared to wild-type plants.

Stvb-i, a Rice Gene Conferring Durable Resistance to Rice stripe virus, Protects Plant Growth From Heat Stress.

Disease resistance is affected by temperature. A rice gene, Stvb-i, is known to have conferred sustained resistance to Rice stripe virus (RSV) despite global warming. Stvb-i protects plants from growth stunting caused by RSV. The underlying resistance mechanism is unclear. Here, Stvb-i showed stable RSV resistance for 20 years in laboratory experiments. This gene encodes a protein distinct from well-studied plant disease-resistance proteins. It has a domain homologous to the histidine kinase/heat-shock protein 90-like ATPase superfamily. Rice has three paralogous genes including Stvb-i. The genes are expressed mainly in meristematic tissues. In the initial period after viral inoculation, RSV multiplication enhanced Stvb-i, whereas Stvb-i suppressed RSV multiplication. Stvb-i silencing inhibited plant growth regardless of viral infection, and silencing of the other paralogous gene that located closely to Stvb-i caused morphological abnormalities. The results suggested that the Stvb-i and its paralogs are related to plant development; especially, Stvb-i supports meristem growth, resulting in plant growth stabilizing. Growth stunting in the Stvb-i–silenced plants was more severe under repetitive heat stress, suggesting that Stvb-i contributed to the attenuation of heat damage in plant development. The symptoms of RSV infection (chlorosis, wilting, stunting, fewer tillers, and defective panicles) were similar to those of heat damage, suggesting that RSV multiplication induces heat-like stress in meristematic cells. Our findings suggest that the mechanism of meristem growth protection conferred by Stvb-i allows plants to withstand both heat stress and RSV multiplication. The suppression of RSV multiplication by the Stvb-i function in meristems results in durable resistance.

Pathophysiologic insight into MesoAmerican nephropathy.

Mesoamerican nephropathy (MeN) is an emerging pathophysiological entity of Chronic kidney desease (CKD) not related to traditional risk factors (diabetes and hypertension) that have caused thousands of deaths in Central America, mainly in sugarcane workers. The focus of this review is to discuss the risk factors and probable mechanisms involved in the initiation and progression of this devastating disease. Frequent episodes of subclinical Acute kidney injury caused by repetitive heat stress, dehydration, and strenuous work have been regarded as the main risk factors for MeN. The combination of them chronically activates vasopressin, renin angiotensin aldosterone system, and polyol-fructokinase pathway in the kidney. Also, subclinical rhabdomyolysis compound the framework of the disease by exacerbating systemic inflammation and inducing uricosuria. Exposure to nephrotoxins, high fructose intake, and use of NSAIDs could also contribute to further accelerating the progression of the disease. The evidence supports the notion that recurrent cycles of heat stress, dehydration, and strenuous work may cause CKD. The chronic activation of such mechanisms likely occurs in other conditions of reduced water intake and probably explains why the current management of CKD has not been effective to revert or halt the progression to end-stage CKD.

Development of an oxidative stress model in weaned pigs highlighting plasma biomarkers' specificity to stress inducers1

To determine the effects of vaccination, heat stress, and dietary antioxidant concentration and investigate some blood parameters as an effective model of oxidative stress, 360 weaned piglets (8.7 ± 1.6 kg) were randomly affected to eight groups in a 2 × 2 × 2 factorial design. Double vaccination at weaning against porcine circovirus type 2 (PCV2) and porcine influenza, heat stress at d 9, 10, 23, 24, 37, and 38 (37°C over a 6 h period), or controls were applied to piglets that were given from weaning to d 14 NRC (2012) levels for vitamin E and selenium or extra supplementation in vitamin E, selenium, and superoxide dismutase–rich melon supplement. Blood samples were taken from 6 piglets per treatment at d 13 and 40, and serum haptoglobin, plasma glutathione peroxidase (GPx), and blood lipid peroxides were determined. Half-hemolysis time (HT50) of red blood cells (RBC) exposed to a controlled free radical attack were determined in whole blood and RBC concentrate. Both vaccination and heat stress decreased ADG (P < 0.05) during phase 2 period (d 14 to 41). Antioxidant supplementation increased HT50 of whole blood at d 13 (P = 0.01) and RBC at d 40 (P = 0.03) and GPx activity at d 13 and 40 (P < 0.01 and P = 0.02, respectively). Vaccination decreased GPx activity (P = 0.04, repeated measures analysis) and resulted in higher concentrations for haptoglobin at d 13 (P < 0.01) and 40 (P = 0.03) and lipid peroxides at d 13 and 40 (P = 0.02). Moreover, exposing vaccinated piglets to repetitive heat stress periods reduced their whole blood and RBC resistance (P < 0.01) at d 40 after weaning. In summary, oxidative stress biomarkers were associated with each specific stress inducer, and cumulative effects of heat and vaccination stressors associated with pig weaning produced responses for all selected biomarkers.

A study of regenerative ability of liver after repetitive heat stress induced liver injury

Background: It is well known that heat stress produces liver injury. It is also known that liver regenerate after injury. This way, there should be almost no or minimal alteration in the size of the liver after regeneration. Aims & Objective: In the present study, after heat induced liver injury, the ability of liver to regenerate itself was assessed. Liver injury was assessed by biochemical [Serum Glutamic Pyruvate Transaminase (SGPT); Serum Glutamic Oxaloacetic Transaminase (SGOT); and Alkaline Phosphatase (ALKP)], morphological, and morphometric changes. On the other hand, Liver regeneration was evaluated by morphological and morphometric observations of male adult albino rats (Wistar strain). Material and Methods: The experimental animals were subjected to repetitive heat stress for 4 hours daily, at 37 ± 0.5 ˚C in a Biological Oxygen Demand (BOD) incubator (relative humidity 65 - 82%) for 2 and 5 consecutive days. Biochemical assessment was done on blood collected from left ventricle of beating heart of rats. Morphometric and morphological studies were conducted under light microscope on paraffin sections (H&E) of liver from control and experimental animals. The morphometric analysis was done by intersection – point counting method, using simple square lattice test system. Relative Liver Wet Weight of all animals was calculated. Results: Progressively degenerative changes in morphological observations (disruption of cell plates in liver lobules and Kupffer cell hyperplasia), progressively increased statistical significance of morphometric (numerical density of Kupffer cells on area - Nak), and biochemical parameters informed that increasing liver damage was present with increased repetition of heat exposures in 2 and 5 days heat exposed experimental albino rats. With this liver degeneration, Relative Liver Wet Weight of all the experimental animals should have been decreased but it was not, reiterating about well-known fact of regenerative ability of liver. Along with progressive changes of heat induced liver injury, progressively increasing regenerative changes were also evident on morphological (binucleate cells and anisocytosis) observations supported by statistically significant morphometric (volume density of hepatocytes – Vvh and numerical density of hepatocytes - Nvh) parameters in experimental animals. Conclusion: The above findings suggested that the regenerative ability of liver progressively increased with progressively increasing liver injury.

Behavioral changes in albino rats due to repetitive heat stress of moderate level

Background: There are a number of studies showing the effect of severe heat stress on behaviour. Severe heat stress has been well reported to cause changes in activity level, attitude/mood, and behaviour. But, the effect of repetitive heat stress of moderate level on all these parameters has not been studied extensively. Aims & Objective: In the present study, the effect of repetitive heat stress of moderate level was assessed on activity level, attitude / mood, and behaviour (spontaneous and provoked) of adult albino male rats (wistar strain). Material and Methods: The experimental animals were subjected to repetitive heat stress for 4 hours daily, at 37±0.5oC in a Biological Oxygen Demand (BOD) incubator (relative humidity 65-82%) for five consecutive days. Daily changes were assessed in activity level during and after heat exposure and in attitude / mood along with behaviour (both spontaneous and provoked) after heat exposure in experimental animals and compared with control animals. Results: There was increased restlessness during heat exposure and decreased level of activity after heat exposure in experimental animals. The mood of the experimental animals was depressed and the experimental animals kept them isolated and did not respond on provoking after heat stress. Conclusion: All the above observations confirmed that exposure to repetitive heat stress, even of moderate level, causes significant change in behaviour of male albino rats.

Assessment of liver damage in male albino rats after repetitive heat stress of moderate level

Background: There are multiple studies showing the effect of severe heat stress on systemic functions. Severe heat stress has been known to affect almost every organ in the body. It is well proved that liver is the organ which is severely affected by heat stress and the biochemical, morphological, and morphometric changes of liver following severe heat stress are well documented. But, the effect of repetitive heat stress of moderate level on the liver has not been studied extensively. Aims & Objective: In the present study, the effect of repetitive heat stress of moderate level was assessed on biochemical [Serum Glutamic Pyruvate Transaminase (SGPT); Serum Glutamic Oxaloacetic Transaminase (SGOT); and Alkaline phosphatase (ALKP)], morphological, and morphometric changes of liver of adult albino male rats (wistar strain). Materials and Methods: The experimental animals were subjected to repetitive heat stress for 4 hours daily, at 37 ± 0.5oC in a Biological Oxygen Demand (BOD) incubator (relative humidity 65 - 82%) for 2, 5, and 10 consecutive days. Biochemical assessment (SGPT, SGOT, and ALKP) was done on blood collected from left ventricle of beating heart of rats. Morphometric and morphological studies were conducted under light microscope on paraffin sections (H&E) of liver from control and experimental animals. The morphometric analysis was done by intersection – point counting method, using simple square lattice test system. Results: The serum levels of liver enzymes were elevated in all heat exposed animals (statistically significant in five and ten days exposed animals) in comparison to controls. Morphological changes of anisocytosis at some sites, disruption of cell plates in lobules, mild Kupffer cell hyperplasia were present in rats exposed to heat for two consecutive days. After five days heat exposure ballooning degeneration, single cell necrosis along with small foci of necrosis disrupting cell plates in lobules, and sinusoidal compression were noticed. Kupffer cell hyperplasia was observed. At various sites, hepatocytes showed regenerative changes as binucleate cells and anisocytosis. After 10 days exposure, changes became more marked. The volume density of hepatocytes (Vvh) and numerical density of hepatocytes (Nvh) increased with the increase in heat exposure, despite increasing degenerative changes, confirming regenerative power of liver by hepatocyte proliferation. The increasing numerical density of Kupffers cells on area (Nak) indicated progressive liver damage. Conclusion: All the observations confirmed that exposure to repetitive heat stress, even of moderate level, leads to liver damage.