It is known that various chemical, physical and physiological stressors can result in stress situation that upset the functional homeostasis. One such situation is termed as oxidative stress (Kodrik D., et al 2015). Concept of oxidative stress emerged in 1985 in reference to imbalance between oxidant and antioxidant (Sies H. 2015). Mild oxidative stress can be helpful to insect but when concentration of oxidant (ROS) increases it leads to damage on protein, lipid and DNA (Kagan varyer 2023). Causes of oxidative stress in insect are environmental factors, xenobiotic degradation, plant phenolic compounds and insecticide like IGR, OP's (Chaitanya R. K. 2016). It has been proved by scientist that insecticide like organophosphate, pyrethroid (Gupta A., 1999 and Kale M., 1999) and even bio insecticide Bt also have the mechanism of oxidative damage to cell (Muita B K and Baxter S W 2023). The damage of most pesticides is represented via the level of lipid peroxidation and GSH depletion (antioxidant), leading to oxidative damage in insect tissues (Ahmad S., 1995). Insect hormones like neuro-hormones, ecdysteroid and juvenile hormone trigger the defense mechanism and maintain the homeostasis in insect body by regulation of anti-stress reaction including oxidative stress (Kodrik et al 2015). Oxidative stress induced by insecticide is also studied in non-target organism by depletion of antioxidant level.
Introduction
Per century, several hundred pesticides have been used in agricultural practices in order to enhance the food production by eradicating insect and controlling the disease vector, and these pesticides differ greatly in their mode of action and toxicity in insect and to non-target organism (Satyanarayan P. V. V. et al 2023). It is known that various chemical (pesticides, drugs, metals, smog, abnormal oxygen concentration, etc.), physical (radiation, temperature, noise, vibration, etc.), and physiological (diseases, injury, aging, inflammation, etc.) stressors can result in a stress situation that may upset functional homeostasis. One such situation is termed oxidative stress (Kodrik D., et al 2015). It has been proved by scientists that insecticide like organophosphate, pyrethroids (Gupta A., 1999 and Kale M., 1999) and even bio insecticide Bt also have the mechanism of oxidative damage to cell (Muita B K and Baxter S W 2023).
Concept of oxidative stress first emerged in 1985 in reference to imbalance between oxidant which attacks the cell and antioxidant responsible for defending it, leading to disruption in redox signaling and control and thus causing molecular damage (Sies 2015). Oxidative stress can be defined as disturbance in balance between the productions of reactive oxygen species (ROS) and antioxidant defenses.
What is ROS?
ROS are free radicals which are important for cellular functions generated in different biological processes. A free radical is unstable and highly reactive and contains one or more unpaired electrons, and is involved in the regulation of various mechanisms and intracellular signaling. ROS also induce cellular senescence, apoptosis, and cell growth regulatory pathways. ROS are generated as by-products of aerobic respiration where the superoxide anion (O2-) and H2O2 are formed when molecular oxygen chemically oxidizes electron carriers. Cellular sources of ROS are produced by the action of different oxidative enzymes, which includes plasma membrane NADPH oxidase (nicotinamide adenine dinucleotide phosphate), intracellular cytosolic xanthine oxidase, peroxisomal oxidases, endoplasmic reticular oxidase and mitochondrial electron transport component.
What is Antioxidant?
Antioxidants are compounds that can stabilize the ROS. These molecules are scavengers for free radicals and get easily oxidized. Antioxidants donate their electron to stabilize the free radicals and make them stable compounds so as to minimize the harmful effect of free radicals. The effects of oxidative stress are mitigated by an endogenous antioxidant enzyme network (Rindler et al., 2013). In insects, the antioxidant defense system consists of enzymatic antioxidants such as catalase (CAT), glutathione-S-transferase (GST) and superoxide dismutase (SOD) as well as nonenzymatic antioxidants such as glutathione (GSH) and ascorbic acid which can withstand the deleterious effect of ROS (Felton, 1995).
The types of antioxidants include: 1) Enzymatic antioxidant or intracellular Antioxidant — SOD (superoxide dismutase), catalase, glutathione peroxidase and glutathione reductase. 2) Non-enzymatic antioxidant — Beta carotene, ascorbic acid. 3) Metabolic antioxidant — GSH, uric acid, transferrin (W.Hasan et al 2017).
The oxidative destruction of lipids acts in a chain reaction to form lipid hydro peroxides (LPO), which can decompose to malondialdehyde (MDA) as an end-product. So, MDA is one of the most frequently used indicators of lipid peroxidation. GSH constitutes a second line in insect immunity through detoxification and metabolizing of toxins in insect body besides protecting insects from the concomitant oxidative stress (Kumar et al., 2003). GSTs play an important role in the detoxification and metabolism of many xenobiotic and endobiotic compounds (Krishnan and Kodrík, 2006). GST conjugates xenobiotic with reduced glutathione for excretion and may eliminate organic hydro peroxide from cells and defend cells from potential damage caused from the products of lipid peroxidation. CAT has the ability to consume hydrogen peroxide (H2O2) at high concentration and quickly converts it to water and oxygen.
How ROS is Helpful to Insect
The moderate oxidative stress can be beneficial; excessive ROS production can harm insects by damaging cellular components. The delicate balance between ROS production and antioxidant defenses determines whether oxidative stress is advantageous or harmful.
Immune Response Enhancement: ROS play a crucial role in the insect immune system. When insects encounter pathogens (such as bacteria or viruses), their immune cells produce ROS to eliminate the invaders. This process helps protect insects from infections and diseases.
Metamorphosis and Development: During metamorphosis (e.g., from larva to pupa to adult), insects experience oxidative stress. Controlled levels of ROS are essential for tissue remodeling, cell differentiation, and overall development. For instance, ROS are involved in breaking down larval tissues during pupation and shaping adult structures.
Adaptation to Environmental Changes: ROS act as signaling molecules, influencing gene expression. Insects exposed to stressors (e.g., temperature fluctuations, UV radiation) adapt by adjusting their gene expression patterns. This adaptation helps them thrive in diverse habitats (Anonymous 2023).
Antioxidant Defense Mechanisms: Insects have evolved sophisticated antioxidant defense systems to counteract oxidative stress. These systems include enzymes like superoxide dismutase (SOD), catalase, and glutathione peroxidase. When ROS levels rise, these enzymes kick into action, maintaining a delicate balance.
Detoxification: Insects encounter various environmental toxins (e.g., pesticides, pollutants). ROS help activate detoxification pathways by inducing specific genes. In this way, oxidative stress contributes to insect survival by aiding in toxin elimination.
Longevity and Stress Resistance: Paradoxically, mild oxidative stress can extend an insect's lifespan. It activates stress response pathways (such as the insulin/insulin-like growth factor signaling pathway) that enhance longevity. Additionally, hormesis — a phenomenon where low levels of stress improve overall resilience — applies to insects as well (Anonymous 2023).
Oxidative Damage and its Impact on Cell
ROS are connected with beneficial effects but are also detrimental because they produce free radicals which can damage DNA, protein and lipid (Kagan varyer 2023).
1. Protein: Reactive oxygen species (ROS) can induce oxidative modifications in proteins by attacking specific amino acids within the cell. These modifications have the potential to alter the natural conformation of proteins, thereby impacting the normal functioning of various biological processes within the cell. The occurrence of oxidative damage to a protein can lead to disruptions in fundamental processes such as cellular signal transduction and metabolism (Zhang et al., 2016).
2. Lipids: Oxidative stress can cause lipid molecules in cell membranes to undergo lipid peroxidation. ROS-targeted lipids may cause changes to the membrane's lipid constituents, which would lessen the cell membrane's selectivity and flexibility. As a result, the cell membrane's regular processes are interfered with, making it more difficult for the cell to connect with its environment. This condition may make it difficult for the cell to react effectively, which could cause disruptions to cellular processes and the incapacity of the cell to send out different biological signals. It might potentially cause cell death by compromising the integrity of the cell membrane (Su et al., 2019).
3. Nucleic Acids (DNA and RNA): Reactive Oxygen Species (ROS) can interact with nitrogenous structures present in the DNA and RNA chains, which constitute the genetic material, by attacking nucleic acids within the cell. As a result of this interaction, disruptions in base pairs, breaks in DNA chains, and cross-linking can occur. Such damages can significantly compromise the integrity of the genetic material, impair the normal functioning of genes, and lead to disruptions in the biological processes of cells (Wang et al., 2023). Consequently, important cellular functions can be greatly impacted by ROS's effect on nucleic acids (Qi et al., 2023).
4. Mitochondria: Oxidative stress can have negative effects on the electron transport system (ETS) and ATP synthesis in mitochondria. Mitochondria utilize oxygen as the final electron acceptor through the electron transport system. This process leads to the formation of highly reactive by-products called superoxide (O2-). Briefly, mitochondria serve as one of the metabolic sources of reactive oxygen species (ROS) production (Snezhkina et al., 2019). Mitochondrial DNA can be damaged by ROS because it has the ability to damage both inner and outer membranes of mitochondria. ROS also have the ability to release cytochrome c, which leads to death of cell.
Causes of Oxidative Stress in Insect
1. Environmental Stress: UV radiation can generate oxidative stress in insects and destroy the functional activity of protein. The toxicity of ultraviolet (UV) light has been reported in various insect pests (Wang W., 2020). Insects faced with cold stress change their cellular metabolism, which often results in increased accumulation of ROS by mitochondria (Anonymous 2022). According to William C. M. et al (2011), cold exposure will cause oxidative stress and that FTRs (fluctuating thermal regimes) would reduce the amount of chill injuries, via activation of the antioxidant system. Increased severity of cold exposure caused a decrease in the glutathione pool. Environment also has a major role in the production of stress because of different pollutants like air, soil, and water. Majority of these compounds used in industry and agriculture have been shown to induce oxidative stress by generating ROS in non-target species including invertebrates (Ahmed s., 1995).
2. Blood-Feeding Insects: Insects which feed on human blood face severe oxidative stress due to the release of iron from hemoglobin. This iron release can potentially induce oxidative damage and even lead to death of insect. E.g. Mosquito (Kirkinezos, I.G. and C.T. Moraes 2001).
3. Metabolism and Respiration: Insects engage in metabolic processes and respiration, which generate ROS as by-products. These highly reactive molecules can damage cellular components (Chaitanya R. K. 2016).
4. Xenobiotic Degradation: Insects metabolize xenobiotic through microsomal oxidation, resulting in ROS production. E.g. Honey bee (Chaitanya R. K., 2016).
5. Effect of Phytochemical, Herbicide and Insecticide: Plant phenolic compounds, such as flavonoids and tannins, which are involved in plant defense mechanism, can produce free radicals in herbivorous insects (Sakihama, Y., et al., 2002). The midgut of insect is a highly oxidizing environment. Hence in lepidopteran larvae, Helicoverpa zea and Spodoptera littoralis, phenolic acids were found to increase various indicators of oxidative stress in gut tissues (Krishnan, N. and F. Sehnal 2016). Herbicides like paraquat are well known to generate oxidative stress in insect species (Sakihana y., et al 2002). Insect growth regulator (IGR) is a substance (chemical) that inhibits the life cycle of an insect and has been used to control the insect pests. Hormonal IGRs typically work by mimicking or inhibiting the juvenile hormone (JH) or ecdysone. Studies on IGRs like Applaud (buprofezin) as a chitin synthesis inhibitor and Admiral (pyriproxyfen) as juvenile hormone analog (JHA) in the larval body of the cotton leaf worm, S. littoralis, resulted in the occurrence of lipid peroxidation in the larval tissues which enhanced different anti-oxidant defensive systems including malondialdehyde (MDA) and glutathione reduction (Nedal M.F., 2012).
Hormonal Regulation of Oxidative Stress
To avoid or at least reduce oxidative stress, organisms have developed effective defense systems controlled by nervous and endocrine centers. In mammals, the stress response pathways are controlled from the hypothalamic–pituitary brain center with the help of a suite of corresponding hormones. In insects there are different hormones to regulate the different functions like juvenile hormone, ecdysteroid and neuro-hormones. One of the best investigated groups of insect hormones is the so-called adipokinetic hormone/red pigment-concentrating hormone family (AKH/RPCH family).
1. AKH (Adipokinetic Hormones): AKHs are metabolic neuro hormones that trigger defense reactions and are responsible for maintaining homeostasis in the insect body by controlling anti-stress reactions, including those responsible in counteracting OS. Adipokinetic hormones (AKHs) are secreted from the corpora cardiaca — a small neuroendocrine gland connected with the brain. The balance between the OS and its control by AKHs was attained by feedback regulation between an oxidative stressor and AKH actions. The effect is reported for paraquat (Vecera J et al 2007), Galanthus nivalis agglutinin and Bacillus thuringiensis toxin (Kodrik D 2007) and also for endosulfan and malathion (Velki M et al 2011) insecticides with an OS effect. It was suggested that the activation of protective antioxidative mechanisms is derived from the effect of oxidative stressors on AKH level in the insect body (Chaitnaya R. K. 2016).
2. Juvenile Hormone: JHs are synthesized and secreted from the corpora allata in the insect brain. Recent studies have implicated that lack of JH may confer resistance to OS. The elimination of JH synthesis extended the survival of flies exposed to hydrogen peroxide. The survival times returned to those in control when the knockout flies were treated with JH analog methoprene. Moreover, another JH analog, pyriproxyfen, induced OS in the wax moth Galleria mellonella, as the antioxidative enzyme activities, CAT and SOD, increased after the pyriproxyfen application. Similarly, pyriproxyfen increased the activity of enzymes CAT and GST, as well as the accumulation of MDA and GSH, in larvae of S. littoralis. JHs are also involved in the control of antioxidative reactions albeit indirectly via the regulation of vitellogenin and transferrin synthesis (Chaitanya R. K. 2016).
3. 20-Hydroxyecdysone (20E): In D. melanogaster, ecdysone-induced methionine sulfoxide reductase A enhances resistance to hydrogen peroxide (Roesijadi G., et al 2007). It also regulates the methionine sulfoxide reductase enzyme expression via the ecdysone receptor (EcR-UPS) complex. Treatment with insect 20E protected mammals against cerebral ischemia injury by inhibiting production of ROS/RNS and modulating OS-induced signal transduction pathways. Treatment of B35 rat neuroblastoma cells with hydrogen peroxide led to OS-induced apoptosis, mitochondrial membrane potential dissipation, neuronal injury, generation of intracellular ROS/RNS, decrease of cellular antioxidant potential, and increase of lipid peroxidation, all of which were significantly eliminated by 20E (Kodrik, D., et al 2015).
Oxidative Stress and Insecticide
Pesticides are important chemicals that deter or kill pests. Pesticides can be grouped into different chemical families, such as organochlorines, organophosphates, organofluorines, carbamates, pyrethroids, bipyridyl herbicides, triazine herbicides, triazoles, and chloroacetanilide herbicides (Georgiadis N., et al 2018). As the population of the globe is increasing, demand for food needs to be met and around the 1950s the green revolution was initiated in Mexico to increase agricultural production. Since then a number of pesticide compounds were manufactured and marketed widely irrespective of their hidden potential towards adverse health effects (Abdolahi M., et al. 2004).
The use of pesticides has continued to increase as it is still considered the most effective method to reduce pests and increase crop growth. However, pesticides have other consequences, including potential toxicity to humans and wildlife. Pesticides have been associated with increased risk of cardiovascular disease, cancer, and birth defects. Based on experimental evidence, various types of pesticides all seem to have a common effect: the induction of oxidative stress in different cell types and animal models. Pesticide-induced oxidative stress is caused by both reactive oxygen species (ROS) and reactive nitrogen species (RNS), which are associated with several diseases including cancer, inflammation, and cardiovascular and neurodegenerative diseases (Sule R.O. et al 2022).
Different classes of pesticides may induce in vitro and in vivo generation of ROS. The damage of most pesticides is represented via the level of lipid peroxidation and GSH depletion, leading to oxidative damage in insect tissues (Ahmad, 1995). Oxidative stress is associated with exposure to several organophosphorus compounds and different pyrethroids (Chaitanya R. K. 2016).
Insecticide Groups Associated with Oxidative Stress
1. Pyrethrins and Pyrethroids: Pyrethrins are natural insecticides derived from yellow Chrysanthemum cinerarifolium and Tanacetum cinerariifolium, and are among the oldest known insecticides, first used in the 1800s. Numerous synthetic derivatives known as pyrethroids have been produced, with greater chemical stability than the natural pyrethrins. Pyrethrin and pyrethroid aerosols are frequently used as automated insect sprays in public areas. Pyrethroid pesticides show high toxicity to a wide range of insects and low toxicity to mammals and birds, and rapid biodegradability. However, the liberal use of pyrethroids has increased the risk of intoxication for non-target species, such as birds, animals and organisms present in soil and water. Pyrethroids exert their insecticide effects through delaying closure of the inward sodium channel of the nerve membrane. Several studies have indicated that pyrethroids induce oxidative stress (Gupta A., 1999 and Kale M., 1999). The increase content of antioxidant enzymes, such as superoxide dismutase and catalase, which decomposes H2O2, and glutathione (GSH) in erythrocytes is probably an initial adaptive response to increased oxidative stress in pyrethroid intoxicated rats (Kale M., et al 1999).
2. Organophosphates: Organophosphates (OP) are cholinesterase-inhibiting chemicals used predominately as pesticides. They are also used as chemical warfare agents (nerve agents). OPs include all insecticides containing phosphorous derived from phosphoric acid, and are generally the most toxic of all pesticides to vertebrate animals. OPs and carbamates inhibit the function of carboxylic ester hydrolases, such as chymotrypsin, acetylcholinesterase (AChE), plasma or butyrilcholinesterase (BuChE), plasma and hepatic carboxylesterases (aliesterases), paraoxonases (asterases), and other nonspecific esterases within the body. The most prominent clinical effects of poisoning with OPs result from their inhibition of AChE. Several studies have demonstrated oxidative stress induced by OPs in rats and humans (Ranjbar A., et al, 2003). Lipid peroxidation is also evident in rat brains and human erythrocytes (Gultekin F., 2000). OP-induced seizures have been reported, associated with oxidative stress. It has also been shown that acute tubular necrosis which accompanies OP toxicity is related to reactive oxygen species and lipid peroxidation (Abdollahi M., et al 2004).
3. Organochlorines: The organochlorines are insecticides that contain carbon, chlorine and hydrogen. They are also referred to as chlorinated hydrocarbons, chlorinated insecticides and chlorinated synthetics. The organochlorine insecticides may be divided into four distinct groups, including: DDT (dichlorodiphenyltrichloroethane) and related analogs (methoxychlor); cyclodienes (aldrin, endrin, heptachlor, dieldrin, chlordane, endosulfan, chlordecone); hexachlorocyclohexane (lindane); and related compounds. Because they are so lipid soluble, these compounds are stored in fatty tissues, and repeated small exposures may result in accumulation and eventual clinical toxicity. DDT use was banned in the 1960s due to its hazards to the environment. Several studies have demonstrated that DDT and methoxychlor induce oxidative stress and lipid peroxidation (Gupta R. C. 2001). Hexachlorocyclohexane (HCH) is the only organochlorine insecticide which is still widely used against pests and scabies. HCH is metabolized by the smooth endoplasmic reticulum cytochrome P450 system. Lipid peroxidation has been proposed as a major molecular mechanism involved in tissue injury induced by lindane. Many studies have shown the oxidative effect of lindane in various organs of mammals, such as rat blood, brain testis and liver — all these effects were duration- and age-dependent (Simon K.A.2002, Sahoo A. 2000 and Sahoo A. 1998).
Case Studies Related to Oxidative Stress
Case Study 1 — Maheshwari N. et al (2022): Oxidative stress, DNA damage and histological alterations in Bombyx mori exposed orally to pesticide Dimethoate. Bombyx mori was used as a model organism to study the effect of commercial formulation of dimethoate (Dimethoate 30% EC) on the gut, silk gland, and fat body tissue at concentrations of 25, 50, and 100 ppm. The results showed that sub-lethal doses of dimethoate caused weight loss and induced damage at the histological level to the mid-gut, silk gland, and fat body of B. mori. It also caused a decrease in the level of antioxidants like CAT, SOD, GPx, GSH, and GST, indicating that dimethoate has produced a shift of ROS balance towards free radical generation and resulted in overall damage to this organism. Sub-lethal doses also caused lipid peroxidation in the silk gland, gut, and fat body of B. mori. The disruption was also seen in the mid-gut and middle silk gland at the DNA level, where it caused single-strand breaks. Damage at histological, biochemical, and molecular levels was most extreme at a concentration of 100 ppm. Conclusion: dimethoate-30% EC in sub-lethal concentrations caused a decrease in antioxidant enzyme levels and resulted in cell membrane damage via LPO. Histological analysis revealed damage to all tissues with hyper-vacuolization and Pyknosis being common defects observed. Thus, dimethoate exposure is harmful to silkworms and, therefore, to sericulture.
Case Study 2 — Satyanarayan P. V, V. et al, (2023): A study of oxidative stress and antioxidant status of agriculture workers exposed to organophosphorus insecticide during spraying. Oxidative stress status and Acetylcholinesterase (AChE) activity were studied in blood samples obtained from 61 agricultural workers engaged in spraying organophosphorus (OP) insecticides in the mango plantation, with a minimum work history of one year, in the age range of 12–55 years. Controls were age-matched, unexposed workers. They were evaluated for oxidative stress markers MDA (end product of lipid peroxidation), reduced glutathione (GSH), and AChE and butyrylcholinesterase (BChE) levels in blood. Results showed a marked inhibition of the AChE and BChE activities in the sprayers as compared to the controls. The malondialdehyde (MDA) level was found to be increased significantly in sprayers (p<0.05), while depletion in the concentration of antioxidant glutathione (GSH) was also observed in the sprayers. Conclusion: An increased level of MDA in exposed pesticide sprayers is probably reflective of increased lipid peroxidation and cell damage (Oxidative stress).
Case Study 3 — Muita B. K., and Baxter S. W. (2022): Temporal exposure to Bt insecticide causes oxidative stress in larval midgut tissue. They challenged transgenic Bt-susceptible Drosophila melanogaster larvae with moderate doses of activated Cry1Ac toxin and assessed the midgut tissues after one, three, and five hours using transmission electron microscopy and transcriptome sequencing. The result shows that larvae treated with Cry1Ac showed dramatic changes to their midgut morphology, including shortened microvilli, enlarged vacuoles, thickened peritrophic membranes, and swelling of the basal labyrinth, suggesting water influx. Transcriptome analysis showed that mitochondria-related genes were strongly upregulated following toxin exposure. Defective mitochondria produced after toxin exposure were likely to contribute to significant levels of oxidative stress. Significant reductions in both mitochondrial aconitase activity and ATP levels in the midgut tissue supported a rapid increase in reactive oxygen species (ROS) following exposure to Cry1Ac. Conclusion: These findings support the role of water influx, midgut cell swelling, and ROS activity in response to moderate concentrations of Cry1Ac.
Case Study 4 — Motta J. V. D. O. et al (2023): Midgut cell damage and oxidative stress in Partamona helleri (Hymenoptera: Apidae) workers caused by insecticide lambda-cyhalothrin. Bees were orally exposed to lambda-cyhalothrin (LC50 = 0.043 mg a.i. L−1) and their midguts were evaluated. The results revealed signs of damage in the midgut epithelium, including pyknotic nuclei, cytoplasm vacuolization, changes in the striated border, and the release of cell fragments. The ingestion of lambda-cyhalothrin led to an increase in the activity of superoxide dismutase and the levels of NO2/NO3 markers indicating oxidative stress. Conversely, the activities of catalase and glutathione S-transferase enzymes decreased, supporting the occurrence of oxidative stress. Conclusion: The insecticide lambda-cyhalothrin is toxic for adult P. helleri workers and damages the midgut epithelium and induces oxidative stress and death in P. helleri workers, providing important information about the hazards associated with this pesticide's toxicity to nontarget organisms, including the stingless bee.
Case Study 5 — Wang Xu et al., 2016: Fipronil insecticide toxicology: oxidative stress and metabolism. Fipronil (FIP) is widely used across the world as a broad-spectrum phenylpyrazole insecticide and veterinary drug. FIP targets the gamma-aminobutyric acid (GABA) receptor and has favorable selective toxicity towards insects rather than mammals. However, because of accidental exposure, incorrect use or widespread FIP use leading to the contamination of water and soil, there is increasing evidence that FIP could cause a variety of toxic effects on animals and humans, such as neurotoxic, hepatotoxic, nephrotoxic, reproductive, and cytotoxic effects. In the last decade, oxidative stress has been suggested to be involved in the various toxicities induced by FIP. The review reports that studies have been conducted to reveal the generation of reactive oxygen species (ROS) and oxidative stress as a result of FIP treatment. Furthermore, the metabolism of FIP was reviewed, and during this process, various CYP450 enzymes were involved and oxidative stress might occur.
Case Study 6 — Nahla M. Abd El-Aziz and Nedal M. F. (2015): Oxidative stress effect of abamectine and hematoporphyrin with the antioxidant efficiency in cotton leaf worm, Spodoptera littoralis. Abamectin (5, 15, 25, 50, 75 ppm) and hematoporphyrin/HP (25, 75, 100, 150, 200 ppm) were tested against 4th instar larvae of S. littoralis using the dipping technique. Treatment with LC50 abamectin and HP increased significantly the concentration of MDA in the larval tissues by 37.73% and 83.42%, respectively on the 1st day post-treatment. Abamectin treatment caused significant decrease in the level of GSH on the 3rd and 4th days post-treatment. CAT was significantly increased in abamectin treated larvae, reaching its maximum level on the 2nd day (199.3%). HP treatment caused a highly significant increase in the activity of CAT reaching its maximum activity on the 1st and 2nd day of treatment by about 126.99 and 200%, respectively. Conclusion: The study demonstrates induction of lipid peroxidation and enhancement of the insect antioxidant system for scavenging ROS resulted from oxidative stress of abamectin and HP.
Conclusion
An overall conclusion of these studies is that insecticide causes oxidative stress (OS) in insect and other non-target organisms. Bt insecticide causes oxidative stress to larval gut. Due to lambda cyhalothrin, midgut cell damage occurs due to oxidative stress in stingless bee. Organophosphate insecticide also causes oxidative stress other than AChE damage. Pyrethroid insecticide also produces oxidative stress.