COVID-19 and waste management in Indian scenario: challenges and possible solutions.

The outbreak of COVID-19 pandemic has created havoc all across the globe causing exponential casualties and tremendous health and economic loss. With increasing COVID-19 cases, the amount of biomedical waste has increased manifolds making more people vulnerable to the pandemic. The developing and underdeveloped countries are already facing the challenges of waste management, and the waste generated during the pandemic scenario has added to the already existing challenges. The improper waste management practices need to be corrected; otherwise, the world will be facing a new disaster that could be termed as 'waste disaster'. The increase in COVID-19-associated waste (CAW) quantity and their availability in the environment will result in their easy approach to other organisms, which will possibly increase the potential risk of food chain contamination. Some of the countries have already started to make backup plans and are struggling to overcome the 'waste disaster'. In light of the limited knowledge available on the mutational properties and possible hosts of this newly emerged COVID-19, there is a great demand to have an efficient strategy to prevent the environment from further contamination in India. The necessity of the prevailing time is to create a more efficient, automatic, mechanized, and well-modified waste management system for handling the present situation and delaying the projected waste disaster in the near future in the era of COVID-19. The article aims to address the issues that originated from waste discharges, their potential sources along with possible sustainable solutions.

Effect of n-propylthiouracil or thyroxine on arsenic trioxide toxicity in the liver of rat.

Involvement of thyroid gland in the hepatotoxic manifestations of arsenic trioxide (As(III)) has been studied in rat. The effects of n-propylthiouracil (PTU) (a thyrotoxic compound) and L-thyroxine (a thyroid hormone) have been studied with reference to T(3) and T(4) values in the serum, arsenic concentration in the liver, Ca(2+) accumulation in the liver, aspartate transaminase, alanine transaminase and bilirubin values as the indicators of liver function, histopathological observations and finally the ultrastructural studies. It is concluded that hypothyroid condition protects against As(III) toxicity. Scavenging of reactive oxygen species (ROS) that significantly contribute in As(III) toxicity, by high intracellular concentration of reduced glutathione, as a consequence of PTU treatment is proposed as the plausible protective mechanism.

Influence of thyroxine and n-propylthiouracil on nephro-toxicity of inorganic arsenic in rat.

The effect of hyper or hypoactive thyroid on the renal toxicity of arsenic trioxide has been studied in rats. It was observed that pre-treatment of rats with thyroxine stimulates arsenic excretion in urine. The anti-thyroid drug n-propylthiouracil (PTU), inhibits the accumulation of arsenic in renal tissue. Both treatments affect the renal pathology. Histopathological lesions are less severe in PTU and arsenic-treated rats in comparison to thyroxine and arsenic-treated rats. Ultrastructural studies support light microscopical observations. An adaptive response was noticed against arsenic in PTU pre-treated rats. We attribute this response to decreased glutathione-S-transferase (GSH) activity and increased GSH synthesis in the kidney. A relationship between thyroidal activity and arsenic toxicity is suggested by present observations.

Effect of arsenic (AsIII) on glutathione-dependent enzymes in liver and kidney of the freshwater fish Channa punctatus.

The possible role of glutathione-dependent enzymes in the liver and kidney of the freshwater fish Channa punctatus has been studied after exposure to arsenic trioxide for different durations. Activities of glutathione-S-transferases, glutathione peroxidase, glutathione reductase, and catalase decreased in the liver and kidney as a result of the initial increase in arsenic concentration in the liver and kidney. However, during longer exposures, a decline in arsenic concentration corresponded with improved enzyme activity. Because arsenic manifests its toxicity by inducing oxidative stress, the antioxidant enzymes, especially the glutathione-dependent enzymes, play a protective role in arsenic toxicity.

Resistance to oxidative stress in a freshwater fish Channa punctatus after exposure to inorganic arsenic.

The biochemical toxicity of arsenic trioxide (AsIII) in a freshwater edible fish Channa punctatus has been studied on exposures ranging from 7 to 90 d. The arsenic concentration increased exponentially in liver, kidney, gills, and muscles of fish up to 60 d of exposure to arsenic. However, arsenic concentration in these tissues declined at 90 d of exposure. This relationship between period of exposure and concentration of arsenic in selected tissues suggests an adaptive response of fish to arsenic. Furthermore, exposure to arsenic-induced lipid peroxidation in these organs increased initially at 7 d of exposure; however, it decreased up to 60 d of exposure but increased again at 90 d of treatment. Values of reduced glutathione (GSH) reflected the observations of lipid peroxidation. The role of GSH in this adaptive response has been discussed.

Oxidative stress by inorganic arsenic: modulation by thyroid hormones in rat.

Arsenic toxicity is attributed mainly to lipid peroxidation and oxidative stress. We therefore studied the modulatory effects of thyroid hormones on arsenic toxicity in rat on lipid peroxidation and oxidative stress. Thyroid hormones, through a mechanism unknown at present, inhibit arsenic accumulation in liver and kidney. Mobilization of arsenic apparently diminishes lipid peroxidation and improves reduced glutathione status, two biochemical demands of combating arsenic toxicity. Results are discussed in reference to the effect of thyroid hormones on microsomal metabolism of arsenic. Arsenic is less toxic in hyperthyroid than in hypothyroid rats. A physiological antagonism between arsenic and thyroxine is discussed.

Inevitable glutathione, then and now.

Glutathione a predominant tripeptide thiol compound of many prokaryotes and eukaryotes, is synthesized from its precursor amino acids eg. gamma-glutamate, cysteine and glycine. It is mainly involved in detoxication mechanisms through conjugation reactions. Other functions include thiol transfer, destruction of free radicals and metabolism of various exogenous and endogenous compounds. It becomes mandatory for a cell to manage high concentration of intracellular GSH to protect itself from chemical/dug abuse. Glutathione dependent enzymes viz: glutathione-S-transferases, glutathione peroxidase, glutathione reductase and gamma-glutamate transpeptidase facilitate protective manifestations. Liver serves as a glutathione-generating factor which supplies the kidney and intestine with other constituents of glutathione resynthesis. The principal mechanism of hepatocyte glutathione turnover appears to be cellular efflux. Kidney too plays an important role in organismic GSH homeostasis. Role of GSH in organs like lung, intestine and brain has recently been described. GSH involvement in programmed cell death has also been indicated. Immense interest makes the then "thee glutathione" as "inevitable glutathione". This article describes the role of this vital molecule in cell physiology and detoxication mechanisms in particular.