Impact of Heavy Metal Stress on Antioxidant Mechanisms of Avicennia marina (Forsk.) and Rhizophora mucronata Lamk.

Mangrove species are growing in exposed areas which have heavy metal contamination. The safeguard the mangrove ecosystem, it is important to understand their antioxidant responses to heavy metal toxicity. The goal of this study was to determine the effect of multi-heavy metals i.e. (Pb, Cd, Cr and Hg) on two mangrove plants Avicennia marina and Rhizophora mucronata of Indus delta via investigating their antioxidative defence mechanism of leaves and roots. In this regard mangrove seedlings of both species were treated with five different concentrations of four heavy metals and different time durations (15, 30, 45 and 60 days) for ascorbate peroxidase, catalase and superoxide dismutase in leaves and root tissues. The findings indicate that the heavy metals have significantly altered the antioxidant enzyme activities with respect of metals concentration and duration of exposure. With extended exposure higher antioxidant activities was observed in metal treated roots and leaves at higher concentrations. A pronounced stimulation (P<0.001) of CAT activity in both roots and leaves of A. marina occurred after 15 days of stress (38.3 and 26.6 µmol/mg protein/min) at 1 MHM. Our analysis also found that roots have shown greater activity in protecting against reactive oxygen species (ROS). Among the roots of two mangroves SOD activity in marina showed better tolerance towards metals stress (9.26 U/mg protein at 15 MHM) compare to mucronata (6.09 U/mg protein at 10 MHM). APX showed maximum stimulation at 20 MHM in leaves (19.130 µmol/mg protein/min) and at 10 MHM in roots (19.02 µmol/mg protein/min) of A. marina after 30 days metals treated plant. Hence, it confirms that the antioxidative defence system plays a critical role in A. marina and R. mucronata to tolerate the multiple heavy metals stress. However, A. marina showed greater antioxidant activity especially catalyst enzyme activity as compared to R. mucronata, which is well evident by its dominancy in the region.

Effect of Chlorpyrifos-Induced Toxicity in Brassica juncea L. by Combination of 24-Epibrassinolide and Plant-Growth- Promoting Rhizobacteria

Pervasive use of chlorpyrifos (CP), an organophosphorus pesticide, has been proven to be fatal for plant growth, especially at higher concentrations. CP poisoning leads to growth inhibition, chlorosis, browning of roots and lipid and protein degradation, along with membrane dysfunction and nuclear damage. Plants form a linking bridge between the underground and above-ground communities to escape from the unfavourable conditions. Association with beneficial rhizobacteria promotes the growth and development of the plants. Plant hormones are crucial regulators of basically every aspect of plant development. The growing significance of plant hormones in mediating plant–microbe interactions in stress recovery in plants has been extensively highlighted. Hence, the goal of the current study was to investigate the effect of 24-epibrassinolide (EBL) and PGPRs (Pseudomonas aeruginosa (Ma), Burkholderia gladioli (Mb)) on growth and the antioxidative defence system of CP-stressed Brassica juncea L. seedlings. CP toxicity reduced the germination potential, hypocotyl and radicle development and vigour index, which was maximally recuperated after priming with EBL and Mb. CP-exposed seedlings showed higher levels of superoxide anion (O2.−), hydrogen peroxide (H2O2), lipid peroxidation and electrolyte leakage (EL) and a lower level of nitric oxide (NO). In-vivo visualisation of CP-stressed seedlings using a light and fluorescent microscope also revealed the increase in O2.−, H2O2 and lipid peroxidation, and decreased NO levels. The combination of EBL and PGPRs reduced the reactive oxygen species (ROS) and malondialdehyde (MDA) contents and improved the NO level. In CP-stressed seedlings, increased gene expression of defence enzymes such as superoxide dismutase (SOD), ascorbate peroxidase (APOX), glutathione peroxidase (GPOX), dehydroascorbate reductase (DHAR) and glutathione reductase (GPOX) was seen, with the exception of catalase (CAT) on supplementation with EBL and PGPRs. The activity of nitrate reductase (NR) was likewise shown to increase after treatment with EBL and PGPRs. The results obtained from the present study substantiate sufficient evidence regarding the positive association of EBL and PGPRs in amelioration of CP-induced oxidative stress in Brassica juncea seedlings by strengthening the antioxidative defence machinery.

The pancreatic beta cell: an intricate relation between anatomical structure, the signalling mechanism of glucose-induced insulin secretion, the low antioxidative defence, the high vulnerability and sensitivity to diabetic stress

The biosynthesis of insulin takes place in the insulin-producing beta cells that are organized in the form of islets of Langerhans together with a few other islet cell types in the pancreas organ. The signal for glucose-induced insulin secretion is generated in two pathways in the mitochondrial metabolism of the pancreatic beta cells. These pathways are also known as the triggering pathway and the amplifying pathway. Glucokinase, the low-affinity glucose-phosphorylating enzyme in beta cell glycolysis acts as the signal-generating enzyme in this process. ATP ultimately generated is the crucial second messenger in this process. Insulin-producing pancreatic beta cells are badly protected against oxidative stress resulting in a particular vulnerability of this islet cell type due to low expression of H2O2-inactivating enzymes in various subcellular locations, specifically in the cytosol, mitochondria, peroxisomes and endoplasmic reticulum. This is in contrast to the glucagon-producing alpha cells and other islet cell types in the islets that are well equipped with these H2O2-inactivating enzymes. On the other hand the membranes of the pancreatic beta cells are well protected against lipid peroxidation and ferroptosis through high level expression of glutathione peroxidase 4 (GPx4) and this again is at variance from the situation in the non-beta cells of the islets with a low expression level of GPx4. The weak antioxidative defence equipment of the pancreatic beta cells, in particular in states of disease, is very dangerous because the resulting particular vulnerability endangers the functionality of the beta cells, making people prone to the development of a diabetic metabolic state.

Energy metabolism in the pancreas of ground squirrels (Spermophilus citellus) during prolonged cold exposure and in hibernation

Mammalian hibernators undergo a host of biochemical adaptations that allow them to survive the harsh cold environment and food restriction. Since the energy metabolism of the pancreas during hibernation remains unknown, we investigated the molecular basis of mitochondrial energy-producing pathways in line with their regulating mechanisms, as well as the (re)organization of antioxidative defence in the pancreas during the prehibernation period and in the hibernating state. To this end, male ground squirrels (Spermophilus citellus) were divided into two groups, the control group kept at room temperature (22±1 °C) and the group exposed to low temperature (4±1 °C). Active animals from the cold exposed group were sacrificed after 1, 3, 7, 12, and 21 days; animals that entered hibernation were sacrificed after 2-5 days of torpor. Our results showed that the protein levels of respiratory complexes I, II, IV and cytochrome c were increased in response to prolonged cold exposure (from day 12) and that such expression profiles were maintained during hibernation. In parallel, AMP-activated protein kinase a (AMPKa) and nuclear respiratory factor 1 (NRF-1) were shown to be upregulated. Moreover, prolonged cold exposure and hibernation induced an increase in the protein expression of antioxidative defence enzymes copper-zinc superoxide dismutase (CuZnSOD) and glutathione peroxidase (GSH-Px). In conclusion, these results point to a controlled metabolic remodeling in the pancreas of ground squirrels during prolonged cold exposure and in hibernation, which includes an improvement of mitochondrial oxidative capacity along with a proportional upregulation of antioxidative defence.