Residual contamination in the environment always has long-time serious consequences for the planet earth. Present study showed the effect of one of the widely used herbicide (Dinotefuran) on mammals when exposed for prolonged period. A comprehensive analysis was conducted.
The first and the most obvious parameter of well-being is weight gain. In developmental studies a strong link was reported between xenobiotic exposure and birth weights. We found a decrease in weight gain, due to probable disruption of hormonal signaling which can ultimately act as a risk factor for metabolic disorders. Dietary interventions improve the situation but to a lesser extent. The duration of the said trial was 90 days so we are not in a position to comment on catch up response of vitamin beyond three months (Svingen T. Ranhoj et al 2018)
Hematological parameters provide better understanding of time dependent side effects of pesticides exposure. Overall reduction in the blood cells (BC) indicate a reduced erythropoiesis or BC destruction. Only white blood cells count increase can point a finger towards a possibility of positive correlation between pesticides toxicity and hematopoietic cancers (Ruifa Hu 2015).
This leukocytosis is also considered as an adaptive measure under stressed condition. Abnormal ESR, can be attributed due to the alteration of plasma proteins. Hematological changes have been reported but conflicting evidence is also present. Regardless of conflicting data abnormality, whether it is in the form of increase or decrease in the blood parameters has been reported persistently (J. L. Del. Prado. Lu 2007). These findings can be due to the disruption of erythropoietic tissue or defensive adaptation, because of less viable circulating cells due to high level of oxidative stress.
Although organophosphates exposure is persistently associated with abnormal low levels of different blood parameters but similar outcomes by Dinotefuran is alarming and require policy revision.
Changes in liver chemistry is always being the first to detect, due to its detoxification role. Liver enzymes are important biomarkers for the assessment of liver function. Any increase or decrease in the activities of these enzymes are indicative of hepato-cellular injury. Abnormal liver function is reflected by the raised values of liver enzymes ALT, AST, ALP as reported by (C. R. Garcia et al 2016), although one conflicting result was reported by (A. A. Malekiand 2013). Liver is the detoxification hub of the body. The changes in the liver biomarkers are well explainable due to liver function of detoxification regarding xenobiotics. It detoxifies xenobiotics by inactivating, removing and transforming them so they can be excreted by intestine or the kidney. Due to persistent or acute heavy exposure, body organs may get overwhelmed, which may lead to the impairment of basic regulatory mechanisms, termed regulatory freeze. This regulatory freeze might induce necrosis and abnormal enzymatic activity. The improvement with the addition of vitamin E can be understand by the notion that ROS-induced oxidative stress was minimized with Vitamin E supplementation that is an antioxidant and maintains redox balance of the body (Miyazawa et al, 2019).
our study is in argument with Garcia et al 2016 except for the values of ALP, abnormal value of ALP along with other parameters suggest a possibility of hepatocellular necrosis which is afterward confirmed by the histopathology carried out in the same study.
Elevated ratio of BUN Creatinine, Cholesterol, and triglycerides are well explained by the fact that oxidative stress has the capacity to impair the vital metabolism of lipids, carbohydrates, and proteins. So oxidative stress linked inflammatory cytokines, along with the adoptive strategies of insulin sensitive tissue like adipose tissues or muscles, collectively create a crisis, which elevate all the parameters. These findings are well supported by the organophosphate’s toxicity studies. However, one lab study conducted by (S. H. Abd 2014) reported low level of cholesterol by exposure to difenoconazole + diclofop methyl in albino rats. Nitrogen containing species, commonly termed as reactive nitrogenous effect (RNS) include NO. Its level is also one of the biomarker of oxidative stress; although less reactive than ROS, but their co-presence with ROS can produce extremely reactive derivatives
From the above findings and discussion, we found that oxidative stress is a plausible explanation for the leading changes in the basic parameters of mammalian system. To elucidate this idea present quantify the oxidative stress by studying cell microenvironment. Vitamin E is a known antioxidant that is thought to prevent cellular damage induced by oxidative stress, the mechanism of reduction in cellular damage is attributed to the potential of vitamin E to inhibit the formation of liquid radicals by preventing liquid peroxidation (LPO) in cell membrane These findings showed that vitamin E treatment had the potential to minimize the deleterious effects of Dinotefuran.
Relationship between environmental exposure of organo-phosphate and oxidative stress is established over the year of research. Pesticides molecule are notably capable of either generating oxidative molecules or can inhibit antioxidant molecules. In the present study as we found elevated levels of cytotoxic biomarkers like H2O, PC, MDA suggested that Dinitofuran is also capable of producing free radicals that can disturb the skin scavenging complex result in lipid peroxidation. The phenomena is supported by the studies conducted by using other organophosphate molecules (Garcia et al, 2016). This interference of antioxidant molecule is supported by the values of vitamin E supplementation group where dietary intake of established antioxidant molecules, show significant improvement in the values of different biomarkers. Increased number of micronuclei has been related to reduce vitality and genome stability. Due to increased number of micronuclei, a genomic chaos is created, as a consequence, genomes tend to reorganize hence become prone to eliminate gene or portion of it ROS are important signaling molecules and contribute significantly as second messengers. Abnormal levels of ROS can cause cell damage even cell death or cell proliferation. Despite their short span of life, ROS can react with biomolecules like lipids proteins, and nucleic acids, resulting in harmful species like lipid adducts and damaged proteins. As a result, these damaged proteins reduce the functionality of enzymes, leading to mutagenicity and carcinogenicity, affecting the tumor micro environment (Kapoor et al 2019). All these findings is verified through histopathology of various tissues, which are in direct correlation with other hematological and cytotoxic parameters.
We can conclude from the present study that like notorious organophosphate, Neonicotinoids has capacity to damage living cells and tissues, if the exposure is persistent even concentration is low. Although further studies with specific reference of Neonicotinoid is required, particularly regarding long term exposure on a population, we recommend policy revision regarding the unintelligent use of herbicides in the developing countries.