Effect of deltamethrin on liver, kidneys and gills oxidative stress and its modulation by α-tocopherol
Fish gills, kidneys and liver are critical organs for their respiratory, osmoregulatory and excretory functions. Respiratory distress is one of the early symptoms of pesticide poisoning. A high rate of absorption of deltamethrin through gills also makes fish a vulnerable target of its toxicity .
Some studies indicated that exposure to lethal concentrations of deltamethrin caused destructive effect in the gill, kidney and liver tissues of C. carpio. The catfish gill is a multipurpose organ that plays role in water gas exchange, osmotic and ionic regulation, acid–base balance and elimination of nitrogenous wastes so, Gill and kidney tissues alterations may result in severe functional problems, ultimately leading to the death of fish.
A single 48 h. exposure to deltamethrin-induced oxidative stress in all the tissues, as depicted by elevated levels of MDA in tissues. Deltamethrin is known to alter cell metabolism in various ways, with a potential genotoxic risk, including DNA damage and micronucleus induction in freshwater fish .
The present findings implicate a role of oxidative stress and free radical formation in these effects. Studies in rodents have demonstrated that absorbed deltamethrin is readily metabolised and excreted; elimination is achieved within 2–4 days. The major metabolic reactions ascribed to deltamethrin metabolism are oxidations mediated by the microsomal monooxygenase system.
The degradation pathways in cows, poultry, and fish are almost similar to those in rodents. However, comparative in vivo and in vitro metabolic studies have shown that fish have a lower capacity to metabolize and eliminate pyrethroid insecticides . This is reflected in the present investigation, where deltamethrin induced peroxidative damage in all the tissues and the gills in particular during a short-term subacute exposure regimen. The extent of MDA is determined by the balance between the production of oxidants and the removal and scavenging of those oxidants by antioxidants .
Gills are the primary sites for the absorption of deltamethrin. It is, therefore, obvious that we noted a high level of MDA coupled with depletion of antioxidant enzymes in the gills. Lipid peroxidation has been extensively used as a biomarker of oxidative stress .
MDA are produced by LPO and considered as indicators of oxidative stress, which results from the free radical damage to membrane components of cells.
Fish exposure to deltamethrin-induced oxidative stress in all tissues, as depicted by elevated levels of MDA in tissues [Table 2). Deltamethrin is known to alter cell metabolism in various ways, with potential genotoxic risk, including DNA damage and micronucleus induction. Comparative in vivo and in vitro metabolic studies have shown that fish have a lower capacity to metabolise and eliminate pyrethroid insecticides .
In the present study exposure of catfish to 0.75 μg/l concentration of deltamethrin (Table 2) shows a marked increase in MDA in the liver, kidney and gill [38, 39]. This marked increase could be attributed to the ability of deltamethrin for free radical formation.
Catalase activity was significantly reduced in the deltamethrin group when compared to control one (Table 3) and this in agreement with Pandey et al.. This significant reduction could be attributed to the influx of super oxide radicals, which have been reported to decrease CAT activity.
The current results showed that deltamethrin is highly toxic to fish even in low concentration [0.75 μg/l) while sublethal concentration of deltamethrin was [1.5 μg/l) as reported by Svobodova et al.. This highly toxic effect of deltamethrin in fish is due to the high rate of absorption of deltamethrin through the gills and lack of fish to the enzymes responsible for metabolism and detoxification of deltamethrin .
The decreased CAT activities, total proteins and albumin, while increased MDA level in liver as well as increased serum AST and ALT activities suggest that deltamethrin produces hepatic dysfunction. The pathogenesis may be through free radical formation where deltamethrin undergoes metabolism in the liver via hydrolytic ester cleavage and oxidative pathways by the cytochrome P450 microsomal enzyme system which probably decreased the P450 contents in liver that may causes in oxidative stress producing depletion of CAT activity and increased the level of MDA leading to hepatic degeneration and necrosis .
α-tocopherol considered the principal antioxidant defence against lipid peroxidation in cell membranes of mammals. The most important role of α-tocopherol in tissues seems to be the protection of membrane PUFA against the effects of oxygen radicals It inhibits peroxidation of membrane lipids by scavenging lipid peroxyl radicals, and is converted into a tocopheroxyl radical as a consequence . α-tocopherol selectively blocks the pyrethroid-modified sodium channel in a dose-dependent manner without affecting normal sodium channels. Moreover α-tocopherol maintained the activities of membrane-bound enzymes at near normal values, and thus preserving mitochondrial membrane integrity and protected some enzyme activities from oxidation by free radicals .
Vitamin E dietary supplementation decreased the susceptibility to lipid peroxidation in rat tissues and peroxidation of rat liver microsomes induced by Fe/ascorbate . The malondialdehyde production in tissue homogenates is used as an estimate of lipid peroxidation.
The protective effect of α-tocopherol against deltamethrin that induced elevation of serum and tissues MDA, observed in this study, was harmony with its antioxidant activity and might also be relevant to its prophylactic and therapeutic effect against environmental pollutants.
ROS have been implicated in the toxicology of pyrethroids, so the protective effect of α-tocopherol, observed in our study, could be important for protecting the different tissues against the oxidative injury following the use of deltamethrin. So fish fed a low level of dietary α-tocopherol failed to counter the stress of deltamethrin pollution.
The results in Table 2 showed that lipid peroxidation in liver was higher than MDA in kidneys and gills also catalase activity were reduced in liver in comparison with kidneys and gills respectively this is due to the fact, that liver is the main organ for metabolism and detoxification of deltamethrin [16, 43], demonstrating that the toxicity of deltamethrin was pronounced in the liver of catfish in compare with kidneys and gills this indicate that liver is the main affected organ by pollution and the most sensitive for oxidative stressors.
In general, antioxidant enzyme activity in kidney and gills was less evident than in liver. Oxidative stress indices (levels of MDA) were significantly higher in liver, despite a trend to increased values were manifested in the remaining tissues. In short, deltamethrin-induced stress responses in different tissues were reflected in the oxidative stress indices and liver function parameters. Those parameters may use as biomarkers for monitoring residual pharmaceuticals in aquatic environment, However more detailed experiments in laboratory need to be performed in the future.
Alterations in serum urea, creatinine (Figures 1 and 2), renal MDA and catalase are encountered primarily in dysfunction and injure of the kidneys, while gill MDA and catalase are markers of gill function.
The hepatic antioxidant enzyme (CAT) activity was inhibited significantly at concentrations (0.75 μg/l) of deltamethrin. Meanwhile, the antioxidant enzyme activity was significantly inhibited in kidney and gills of fish. Moreover there was significant higher MDA level in hepatic, renal and Gill tissues in deltamethrin group compared with control. In short, concentrations of (0.75 μg/l) deltamethrin could induce obvious impacts on different organs in fish, and could affect seriously the health status of fish.
This biochemical information will be helpful in assessing the impact of deltamethrin toxicity to freshwater fish as well as in developing a sensitive biomarker of aquatic pollution caused by the excessive release of deltamethrin into the freshwater.
Alterations of lipid peroxidation and catalase activity after deltamethrin exposure suggesting the use of these antioxidants as a potential biomarker of toxicity associated with contaminant exposure in freshwater catfish.
Application of specific concentration of heavily used deltamethrin with the Egyptian catfish that grow in many water areas, using serum and tissues biochemical makers for monitoring pollution and treatment with natural vitamin E as antioxidant through water and making sure it taken by catfish not forming a film, provides novelty to our study.